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(His)8-Ub-CTAPIII + H2O
(His)8-Ub + CTAPII
-
Ub i.e ubiquitin, CTAPII i.e. connective tissue-activating peptide
-
?
Ac-ALRGG-7-amido-4-trifluoromethylcoumarin
?
Ac-LRGG-7-amido-4-trifluoromethylcoumarin
?
Ac-RLRGG-7-amido-4-trifluoromethylcoumarin
?
activity-based haemagglutinin-tagged ubiquitin + H2O
?
-
-
-
-
?
alpha-tubulin + H2O
?
-
-
-
-
?
beta-tubulin + H2O
?
-
-
-
-
?
branched di-ubiquitin + H2O
ubiquitin
branched dimeric ubiquitin + H2O
ubiquitin
-
-
-
-
?
branched polyubiquitin + H2O
ubiquitin
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
di-ubiquitin + H2O
ubiquitin
EBV ribonucleotide reductase
?
is deubiquitinated by BPLF1 1-246
-
-
?
HCF-1 + H2O
?
HCF-1 is the principal Bap1-interacting protein. It is K48- and K63-ubiquitinated. Endogenous HCF-1C is ubiquitinated at lysine-1807 and/or lysine-1808
-
-
?
head-to-tail dimeric ubiquitin + H2O
ubiquitin
-
-
-
-
?
head-to-tail polyubiquitin + H2O
ubiquitin
-
recombinant substrate from expression in Escherichia coli
-
-
?
hemagglutinin-tagged ubiquitin-vinyl methyl ester + H2O
?
-
-
-
-
?
inhibitor of kappa B-alpha + H2O
?
-
UCHL1 deubiquitinates, thereby resulting in nuclear factor-kappa B inactivation
-
-
?
K48-linked tetraubiquitin + H2O
K48-linked diubiquitin + diubiquitin
-
-
-
-
?
K63-linked polyubiquitin + H2O
K63-linked polyubiquitin + ubiquitin
-
-
-
-
?
linear ubiquitin-beta-galactosidase + H2O
ubiquitin + protein
N2-L-Asp-ubiquitin + H2O
ubiquitin + L-Asp
-
-
-
?
N2-Lys-ubiquitin + H2O
ubiquitin + Lys
-
ubiquitin amide of the alpha amino group of lysine
-
?
N6-(N2-acetyl)Lys-ubiquitin + H2O
ubiquitin + N2-acetyl-Lys
-
ubiquitin amide of the alpha amino group of lysine
-
?
N6-Lys-ubiquitin + H2O
ubiquitin + Lys
Nalpha-(diubiquitin)-[L-Lys] + H2O
?
-
K48 linked diubiquitin
-
-
?
Nalpha-ubiquitin-[MQIFVRPR] + H2O
ubiquitin + MQIFVRPR
-
-
-
-
?
NEDD8-7-amido-4-methylcoumarin + H2O
NEDD8 + 7-amino-4-methylcoumarin
-
-
-
?
NEDD8-protein + H2O
NEDD8 + protein
enzyme shows dual specificity for ubiquitin-conjugates and NEDD8-conjugates
-
?
Nepsilon-(diubiquitin)-[Nalpha-actyl-L-Lys] + H2O
?
-
K48 linked diubiquitin
-
-
?
poly-His tagged di-ubiquitin + H2O
ubiquitin + ?
-
-
-
-
?
polyubiquitin + H2O
ubiquitin
Smad2 + H2O
?
-
weaker association
-
-
?
Smad3 + H2O
?
-
weaker association
-
-
?
Smad7 + H2O
?
-
association with Smad7, which can act as an adaptor able to recruit UCH37 to the type I TGF-beta receptor and reverses Smurf-mediated ubiquitination
-
-
?
spermidine-ubiquitin + H2O
ubiquitin + spermidine
-
-
-
-
?
type I TGF-beta receptor + H2O
?
ubiquitin + H2O
monoubiquitin
-
UCH-L1 removes and recycles ubiquitin molecules from degraded proteins
-
-
?
ubiquitin 7-amido-4-methylcoumarin + H2O
?
-
-
-
?
ubiquitin C-terminal amide + H2O
ubiquitin + NH3
-
-
-
-
?
ubiquitin C-terminal-4-methyl-7-amido-coumarin + H2O
ubiquitin + 4-methyl-7-amino-coumarin
-
UCHL3 is 200fold more active than UCHL1/PGP 9.5
-
-
?
ubiquitin ethyl ester + H2O
ubiquitin + ethanol
ubiquitin ethylester + H2O
ubiquitin + an alcohol
-
synthetic substrate
-
-
?
ubiquitin fused to 60% of its N-terminus + H2O
ubiquitin + 60% of ubiquitin N-terminus
-
recombinant substrate, expressed in Escherichia coli
-
?
ubiquitin glycine methyl ester + H2O
ubiquitin + methanol
-
-
-
-
?
ubiquitin metallothionein + H2O
?
ubiquitin thiol ester of dithiothreitol + H2O
ubiquitin + dithiothreitol
-
-
-
-
?
ubiquitin-4-methylcoumarin 7-amide + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
?
ubiquitin-4-methylcoumarine 7-amide + H2O
ubiquitin + 7-amino-4-methylcoumarine
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
?
-
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
ubiquitin-alcohol + H2O
ubiquitin + alcohol
-
-
-
ir
ubiquitin-alpha-NH-dihydrofolate reductase + H2O
ubiquitin + dihydrofolate reductase
-
-
-
-
?
ubiquitin-alpha-NH-MHISPPEPESEEEEHYC + H2O
ubiquitin + MHISPPEPESEEEEHYC
-
-
-
?
ubiquitin-alphaNH-MHISPPEPESEEEEHYC + H2O
ubiquitin + MHISPPEPESEEEEHYC
ubiquitin-AMC
?
BPLF1 1-246 expresses deubiquitinating activity, cleaves ubiquitin chains linked by K48 and K63
-
-
?
ubiquitin-AMC + H2O
?
-
-
-
?
ubiquitin-B domain of staphylococcal protein-A + H2O
ubiquitin + B domain of staphylococcal protein-A
and variants thereof, substrate is expressed as alpha-linked C-terminal fusion to ubiquitin
-
-
?
ubiquitin-beta1 domain of streptococcal protein G + H2O
ubiquitin + beta1 domain of streptococcal protein G
and variants thereof, substrate is expressed as alpha-linked C-terminal fusion to ubiquitin
-
-
?
ubiquitin-carboxyl extension protein + H2O
ubiquitin + ubiquitin-carboxyl extension protein
ubiquitin-CEP52 + H2O
ubiquitin + CEP52
ubiquitin-CEP80 + H2O
ubiquitin + CEP80
ubiquitin-Cys + H2O
ubiquitin + Cys
-
-
-
?
ubiquitin-Cys-Cys + H2O
ubiquitin + Cys-Cys
-
-
-
?
ubiquitin-Fur4p-conjugate + H2O
ubiquitin + Fur4p
-
ubiquitin is bound to the Fur4p protein via its Lys63
-
?
ubiquitin-human carboxyl extension protein fusion protein + H2O
ubiquitin + human carboxyl extension protein
ubiquitin-magainin + H2O
magainin + ubiquitin
-
is efficiently cleaved at the carboxyl terminus of ubquitin, yielding recombinant magainin with high antimicrobial activity
-
-
?
ubiquitin-peptide + H2O
?
ubiquitin-piscidin 1 + H2O
ubiquitin + piscidin 1
-
-
-
?
ubiquitin-protein + H2O
ubiquitin + protein
ubiquitin-rhodamine110-glycine + H2O
rhodamine110
-
-
-
-
?
ubiquitin-W-G75A + H2O
?
-
-
-
-
?
ubiquitin-W-G76A + H2O
?
-
-
-
-
?
ubiquitin-W-H68A + H2O
?
-
-
-
-
?
ubiquitin-W-I44A + H2O
?
-
-
-
-
?
ubiquitin-W-K11A + H2O
?
-
-
-
-
?
ubiquitin-W-K48A + H2O
?
-
-
-
-
?
ubiquitin-W-K63A + H2O
?
-
-
-
-
?
ubiquitin-W-K6A + H2O
?
-
-
-
-
?
ubiquitin-W-L71A + H2O
?
-
-
-
-
?
ubiquitin-W-L73A + H2O
?
-
-
-
-
?
ubiquitin-W-L8A + H2O
?
-
-
-
-
?
ubiquitin-W-R42A + H2O
?
-
-
-
-
?
ubiquitin-W-R72A + H2O
?
-
-
-
-
?
ubiquitin-W-R74A + H2O
?
-
-
-
-
?
ubiquitin-W-V70A + H2O
?
-
-
-
-
?
ubiquitinyl-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
ubiquitinyl-peptide + H2O
ubiquitin + peptide
ubiquitinyl-Smad2 + H2O
ubiquitin + Smad2
the enzyme de-ubiquitinates both Smad2 and Smad3 and up-regulates their stability
-
-
?
ubiquitinyl-Smad3 + H2O
ubiquitin + Smad3
the enzyme de-ubiquitinates both Smad2 and Smad3 and up-regulates their stability
-
-
?
ubiquitinyldihydrofolate reductase + H2O
ubiquitin + dihydrofolate reductase
-
UCH-1
-
?
wild-type di-ubiquitin + H2O
ubiquitin
-
-
-
-
?
Z-Arg-Leu-Arg-Gly-Gly-7-amido-4-methylcoumarin + H2O
?
-
-
-
-
?
additional information
?
-
Ac-ALRGG-7-amido-4-trifluoromethylcoumarin
?
-
-
-
?
Ac-ALRGG-7-amido-4-trifluoromethylcoumarin
?
-
-
-
-
?
Ac-LRGG-7-amido-4-trifluoromethylcoumarin
?
-
-
-
?
Ac-LRGG-7-amido-4-trifluoromethylcoumarin
?
-
-
-
-
?
Ac-RLRGG-7-amido-4-trifluoromethylcoumarin
?
-
-
-
?
Ac-RLRGG-7-amido-4-trifluoromethylcoumarin
?
-
-
-
-
?
branched di-ubiquitin + H2O
ubiquitin
-
recombinant substrate from expression in Escherichia coli
-
-
?
branched di-ubiquitin + H2O
ubiquitin
-
recombinant substrate expressed in Escherichia coli
-
-
?
branched polyubiquitin + H2O
ubiquitin
-
substrate is ligated to proteins via epsilon-NH-isopeptide bonds
-
?
branched polyubiquitin + H2O
ubiquitin
isopeptide-linked ubiquitin chains
-
?
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
-
i.e. A24, structural chromatin protein, activity of the enzyme is confined to conjugates between ubiquitin and other proteins, formed through epsilon-(alpha-glycyl)lysine bonds
-
?
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
-
best substrate
-
?
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
-
i.e. A24, structural chromatin protein, activity of the enzyme is confined to conjugates between ubiquitin and other proteins, formed through epsilon-(alpha-glycyl)lysine bonds
-
?
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
-
i.e. A24, structural chromatin protein, activity of the enzyme is confined to conjugates between ubiquitin and other proteins, formed through epsilon-(alpha-glycyl)lysine bonds
-
?
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
-
i.e. A24, structural chromatin protein, activity of the enzyme is confined to conjugates between ubiquitin and other proteins, formed through epsilon-(alpha-glycyl)lysine bonds
-
?
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
-
i.e. A24, structural chromatin protein, activity of the enzyme is confined to conjugates between ubiquitin and other proteins, formed through epsilon-(alpha-glycyl)lysine bonds
-
?
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
-
i.e. A24, structural chromatin protein, activity of the enzyme is confined to conjugates between ubiquitin and other proteins, formed through epsilon-(alpha-glycyl)lysine bonds
-
?
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
-
i.e. A24, structural chromatin protein, activity of the enzyme is confined to conjugates between ubiquitin and other proteins, formed through epsilon-(alpha-glycyl)lysine bonds
-
?
conjugate of histone H2A and ubiquitin + H2O
ubiquitin + histone H2A
-
i.e. A24, structural chromatin protein, activity of the enzyme is confined to conjugates between ubiquitin and other proteins, formed through epsilon-(alpha-glycyl)lysine bonds
-
?
di-ubiquitin + H2O
ubiquitin
-
active with wild-type and mutant di-ubiquitin, the latter contains a distal mutant ubiquitin L8A/I44A
-
-
?
di-ubiquitin + H2O
ubiquitin
-
recombinant linear substrate, expressed in Escherichia coli
-
-
?
linear ubiquitin-beta-galactosidase + H2O
ubiquitin + protein
-
recombinant fusion protein co-expressed with the enzyme in Escherichia coli
-
?
linear ubiquitin-beta-galactosidase + H2O
ubiquitin + protein
-
recombinant fusion protein co-expressed with the enzyme in Escherichia coli
-
?
monoubiquitin + H2O
?
-
-
-
-
?
monoubiquitin + H2O
?
-
the octapeptide amide DELRFNAI-NH2 from UCH-L3 binds to monoubiquitin
-
-
?
N6-Lys-ubiquitin + H2O
ubiquitin + Lys
-
ubiquitin amide of the epsilon amino group of lysine
-
?
N6-Lys-ubiquitin + H2O
ubiquitin + Lys
-
ubiquitin amide of the epsilon amino group of lysine
-
-
?
Nedd-8 + H2O
?
-
-
-
?
polyubiquitin + H2O
ubiquitin
-
hydrolysis is restricted to the distal end of the substrate, i.e. ubiquitin farthest from the site of protein attachment in poly-ubiquitin conjugates
-
-
?
polyubiquitin + H2O
ubiquitin
-
active with Lys48-, Lys6-, and Lys11-linked poly-ubiquitins
-
-
?
polyubiquitin + H2O
ubiquitin
-
no activity with poly-ubiquitins that contain a distal mutant ubiquitin L8A/I44A
-
-
?
polyubiquitin + H2O
ubiquitin
-
substrate of UCHL3, no activity with UCHL1/PGP 9.5
-
-
?
polyubiquitin + H2O
ubiquitin
linear chains
-
-
?
polyubiquitin + H2O
ubiquitin
-
dissambly of polyubiquitin
-
?
polyubiquitin + H2O
ubiquitin
-
disassembly of polyubiquitin, terminal step of the proteasome pathway, scheme
-
?
polyubiquitin + H2O
ubiquitin
-
inhibition by prostaglandins of the J series leads to accumulation of polyubiquitins of MW around 250 kDa
-
?
polyubiquitin + H2O
ubiquitin
-
Cezanne deubiquitinates Lys48- or Lys63-polyubiquitinated cellular proteins
-
-
?
polyubiquitin + H2O
ubiquitin
-
substrate of UCHL3, no activity with UCHL1/PGP 9.5
-
-
?
polyubiquitin + H2O
ubiquitin
UCHL5 deubiquitylates the polyubiquitin chain into ubiquitin
-
-
?
polyubiquitin + H2O
ubiquitin
UCHL5 deubiquitylates the polyubiquitin chain into ubiquitin
-
-
?
polyubiquitin + H2O
ubiquitin
-
-
-
?
polyubiquitin + H2O
ubiquitin
-
-
-
-
?
polyubiquitin + H2O
ubiquitin
-
-
-
?
polyubiquitin + H2O
ubiquitin
-
UCHL1/PGP 9.5, overview
-
-
?
polyubiquitin + H2O
ubiquitin
-
-
-
?
type I TGF-beta receptor + H2O
?
UCH37 deubiquitinates and stabilizes type I TGF-beta receptor. Overexpression of UCH37 upregulates TGF-beta-dependent transcription
-
-
?
type I TGF-beta receptor + H2O
?
-
UCH37 dramatically up-regulates TGF-beta-dependent gene expression by deubiquitinating and stabilizing the type I TGF-beta receptor
-
-
?
ubiquitin + H2O
?
-
-
-
-
?
ubiquitin + H2O
?
-
-
-
?
ubiquitin + H2O
?
-
-
-
-
?
ubiquitin + H2O
?
-
-
-
-
?
ubiquitin + H2O
?
-
cleavage of the G76-D77 peptide bond of (L8A, I44A, V70A)-D77 ubiquitin
-
-
?
ubiquitin ethyl ester + H2O
ubiquitin + ethanol
-
-
-
-
?
ubiquitin ethyl ester + H2O
ubiquitin + ethanol
-
-
-
-
?
ubiquitin ethyl ester + H2O
ubiquitin + ethanol
-
-
-
-
?
ubiquitin metallothionein + H2O
?
-
low activity
-
-
?
ubiquitin metallothionein + H2O
?
-
recombinant substrate, expressed in Escherichia coli
-
-
?
ubiquitin metallothionein + H2O
?
-
i.e. UbMT
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
ir
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
recombinant wild-type isozyme L1 and mutants I93M and S18Y
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
fluorogenic synthetic substrate
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
UCH-L1 and UCH-L3
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
ubiquitin makes modest contact with UCH-L1. The interaction is mainly electrostatic, contributed by conserved acidic residues E7, E11, D30, E35, and E37
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
recombinant wild-type isozyme L1
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
-
?
ubiquitin-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
-
?
ubiquitin-alphaNH-MHISPPEPESEEEEHYC + H2O
ubiquitin + MHISPPEPESEEEEHYC
-
-
-
?
ubiquitin-alphaNH-MHISPPEPESEEEEHYC + H2O
ubiquitin + MHISPPEPESEEEEHYC
-
-
-
?
ubiquitin-AW + H2O
?
-
-
-
-
?
ubiquitin-AW + H2O
?
-
poor substrate for UCH-L1
-
-
?
ubiquitin-carboxyl extension protein + H2O
ubiquitin + ubiquitin-carboxyl extension protein
-
UCH-1
-
?
ubiquitin-carboxyl extension protein + H2O
ubiquitin + ubiquitin-carboxyl extension protein
-
carboxyl extension protein of 80 amino acids
-
?
ubiquitin-carboxyl extension protein + H2O
ubiquitin + ubiquitin-carboxyl extension protein
-
carboxyl extension protein of 80 amino acids
-
?
ubiquitin-carboxyl extension protein + H2O
ubiquitin + ubiquitin-carboxyl extension protein
-
carboxyl extension protein of 52 amino acids
-
?
ubiquitin-carboxyl extension protein + H2O
ubiquitin + ubiquitin-carboxyl extension protein
-
carboxyl extension protein of 38 amino acids
-
-
?
ubiquitin-CEP52 + H2O
ubiquitin + CEP52
-
substrate of UCHL1/PGP 9.5, no activity with UCHL3
-
-
?
ubiquitin-CEP52 + H2O
ubiquitin + CEP52
-
substrate of UCHL1/PGP 9.5, no activity with UCHL3
-
-
?
ubiquitin-CEP80 + H2O
ubiquitin + CEP80
-
substrate of UCHL3 and UCHL1/PGP 9.5
-
-
?
ubiquitin-CEP80 + H2O
ubiquitin + CEP80
-
substrate of UCHL3 and UCHL1/PGP 9.5
-
-
?
ubiquitin-human carboxyl extension protein fusion protein + H2O
ubiquitin + human carboxyl extension protein
-
i.e. HUbCEP-52
-
?
ubiquitin-human carboxyl extension protein fusion protein + H2O
ubiquitin + human carboxyl extension protein
-
recombinant substrate, expressed in Escherichia coli
-
?
ubiquitin-peptide + H2O
?
-
-
-
-
?
ubiquitin-peptide + H2O
?
-
-
-
-
?
ubiquitin-peptide + H2O
?
-
-
-
-
?
ubiquitin-peptide + H2O
?
-
UCH enzymes may function to regenerate active ubiquitin from adducts with small nuceleophiles
-
-
?
ubiquitin-peptide + H2O
?
-
-
-
-
?
ubiquitin-protein + H2O
ubiquitin + protein
-
enzyme is crucial for polarization of the actin cytoskeleton, to segregate germline determinants, to assemble an intact cleavage furrow, for cytokinesis and to maintain osmotic balance and execute actin-dependent processes in the early embryo
-
?
ubiquitin-protein + H2O
ubiquitin + protein
enzyme shows dual specificity for ubiquitin-conjugates and NEDD8-conjugates
-
?
ubiquitin-protein + H2O
ubiquitin + protein
important role in regulation of cell growth
-
?
ubiquitin-protein + H2O
ubiquitin + protein
-
-
-
?
ubiquitin-protein + H2O
ubiquitin + protein
-
involved in endocytotic pathway of plasma membrane proteins
-
?
ubiquitin-protein + H2O
ubiquitin + protein
-
Doap4 enzyme form plays a general role in deubiquination of membrane-bound proteins
-
?
ubiquitin-W + H2O
?
-
-
-
-
?
ubiquitin-W + H2O
?
-
competent substrate for both UCH-L1 and UCH-L3
-
-
?
ubiquitin-WA + H2O
?
-
-
-
-
?
ubiquitin-WA + H2O
?
-
poor substrate for UCH-L1
-
-
?
ubiquitinyl-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
mechanistic studies
-
-
?
ubiquitinyl-7-amido-4-methylcoumarin + H2O
ubiquitin + 7-amino-4-methylcoumarin
-
-
-
?
ubiquitinyl-peptide + H2O
ubiquitin + peptide
-
catalyses the hydrolysis of an ester or amide bond involving the C-terminal Gly76 of ubiquitin
-
-
?
ubiquitinyl-peptide + H2O
ubiquitin + peptide
-
catalyses the hydrolysis of an ester or amide bond involving the C-terminal Gly76 of ubiquitin
-
-
?
ubiquitinyl-peptide + H2O
ubiquitin + peptide
-
catalyses the hydrolysis of an ester or amide bond involving the C-terminal Gly76 of ubiquitin
-
-
?
ubiquitinyl-peptide + H2O
ubiquitin + peptide
-
UCH-L3 cleaves peptide extensions of up to 20 residues with high efficiency and low sequence preference
-
-
?
ubiquitinyl-peptide + H2O
ubiquitin + peptide
-
catalyses the hydrolysis of an ester or amide bond involving the C-terminal Gly76 of ubiquitin
-
-
?
additional information
?
-
-
core histones and H1 are not cleaved
-
-
?
additional information
?
-
-
enzyme contains ubiquitin-C-terminal hydrolase activity towards biosynthetic precursors of ubiquitin as well as isopeptidase activity towards ubiquitin histone conjugates as human ubiquitin carboxyl extension protein and ubiquitin C-terminal amide
-
-
?
additional information
?
-
-
purified PGP 9.5 from bovine brain exhibits a specific activity in cleaving ubiquitin-ethylester which is 40% of that shown by bovine thymus UCHL3. UCHL1/PGP 9.5 and UCHL3 hydrolysis rates of various synthetic ubiquitin conjugates compare to rates of hydrolysis of the generic substrate ubiquitin-ethylester. Both enzymes cleave ubiquitin from N-epsilon linked lysine or N-alpha-linked lysine equally well. Neither can cleave the Ub-K48 Ub bond, but both can cleave lysine from the C-terminal of this conjugate. UCHL3 can readily cleave a wide variety of peptides from the C-terminus of ubiquitin if the peptides are less than 20 residues, UCHL1/PGP 9.5 is at least a hundred times less active in this
-
-
?
additional information
?
-
-
core histones and H1 are not cleaved
-
-
?
additional information
?
-
-
uch-L1 may have an important role in the development of neuronal cells in early embryos as well as in the degeneration and disease of neuronal cells in late adult brain. The gene for ubiquitin C-terminal hydrolase L1 is associated with inherited forms of Parkinson's disease
-
-
?
additional information
?
-
uch-L1 may have an important role in the development of neuronal cells in early embryos as well as in the degeneration and disease of neuronal cells in late adult brain. The gene for ubiquitin C-terminal hydrolase L1 is associated with inherited forms of Parkinson's disease
-
-
?
additional information
?
-
-
core histones and H1 are not cleaved
-
-
?
additional information
?
-
-
UCH-1 releases ubiquitins that are conjugated to proteins or adjacend ubiquitin molecules by epsilonNH-isopeptide linkages as well as alphaNH-peptide bonds
-
-
?
additional information
?
-
-
no activity with poly-His-tagged di-ubiquitin
-
-
?
additional information
?
-
-
core histones and H1 are not cleaved
-
-
?
additional information
?
-
no activity with Sentrin-1-conjugates
-
-
?
additional information
?
-
-
no activity with Sentrin-1-conjugates
-
-
?
additional information
?
-
enzyme inhibits cell proliferation
-
-
?
additional information
?
-
-
enzyme inhibits cell proliferation
-
-
?
additional information
?
-
increased activity of neuronal isozyme L1 reduces the risk for Parkinson's disease
-
-
?
additional information
?
-
-
increased activity of neuronal isozyme L1 reduces the risk for Parkinson's disease
-
-
?
additional information
?
-
enzyme regulation
-
-
?
additional information
?
-
-
enzyme regulation
-
-
?
additional information
?
-
-
AMSH is a deubiquinating enzyme with functions at the endosome, it opposes the ubiquitin-dependent sorting of receptors to lysosomes, the enzyme influences the degradation of the EGF receptor by association to endosomes, model of the enzyme's physiological function
-
-
?
additional information
?
-
gene uch-L1 is involved in development of Parkinson's disease
-
-
?
additional information
?
-
-
gene uch-L1 is involved in development of Parkinson's disease
-
-
?
additional information
?
-
-
the enzyme is involved in generation of free monomeric ubiquitin, enzyme deficiency leads is involved in accumulation of ubiquitin and alpha-synuclein leading to aggregation in proteins conforming Lewy bodies and Lewy neurites leading to Parkinson's disease and dementia with Lewy bodies, the enzyme is down-regulated in Alzheimer's disease and in Parkinson's disease, comparison of enzyme expression to general protein synthesis and proteasome activity in brain
-
-
?
additional information
?
-
-
the full length UCH-L1 is a de-ubiquinating enzyme in brain, and a major target of oxidative damage in Alzheimer's diesease and Parkinson's disease brains, modified by cysteine and methionine oxidation and carbonyl formation
-
-
?
additional information
?
-
the full length UCH-L1 is a de-ubiquinating enzyme in brain, and a major target of oxidative damage in Alzheimer's diesease and Parkinson's disease brains, modified by cysteine and methionine oxidation and carbonyl formation
-
-
?
additional information
?
-
-
ubiquitin carboxy-terminal hydrolase L1 activates the P2X receptor leading to potentiation of ATP-induced currents in neurons
-
-
?
additional information
?
-
-
UCH-L1 is involved in Parkinson's disease
-
-
?
additional information
?
-
-
UCH-L1 is involved in Parkinson's disease
-
-
?
additional information
?
-
UCH-L1 is involved in Parkinson's disease
-
-
?
additional information
?
-
-
UCH-L1 regulates the morphology of neural progenitor cells and modulates their differentiation, it mediates and enhances neurogenesis in the embryonic brain
-
-
?
additional information
?
-
-
AMSH interacts with the signal transducing adaptor molecule, STAM, via the SH3-domains
-
-
?
additional information
?
-
-
the enzyme shows de-ubiquinating activity
-
-
?
additional information
?
-
-
oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase L1 associated with idiopathic Parkinsons and Alzheimers diseases
-
-
?
additional information
?
-
oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase L1 associated with idiopathic Parkinsons and Alzheimers diseases
-
-
?
additional information
?
-
-
UCHL1 is an essential gene in cell survival under normal growth conditions and against oxidative stress
-
-
?
additional information
?
-
UCHL1 is an essential gene in cell survival under normal growth conditions and against oxidative stress
-
-
?
additional information
?
-
-
UCHL1 is an essential gene to maintain cell homeostasis under normal growth and oxidative stress conditions
-
-
?
additional information
?
-
UCHL1 is an essential gene to maintain cell homeostasis under normal growth and oxidative stress conditions
-
-
?
additional information
?
-
UCHL1 is associated with Parkinsons disease
-
-
?
additional information
?
-
neither Uch37 alone nor the Uch37-Adrm1 or Uch37-Adrm1-S1 complexes can hydrolyse di-ubiquitin efficiently, rather incorporation into the 19S complex is required to enable processing of polyubiquitin chains
-
-
?
additional information
?
-
-
UCH-L1 may directly destroy or neutralize oligomeric beta-amyloid peptide and may promote degradation of beta- and gamma secretase, or amyloid precursor protein
-
-
?
additional information
?
-
-
wild-type UCH-L1 interacts with multiple proteins over 30 kDa. It shows no interaction with beta-actin
-
-
?
additional information
?
-
Bap1 helps to control cell proliferation by regulating HCF-1 protein levels and by associating with genes involved in the G1-S transition
-
-
?
additional information
?
-
epigenetic inactivation of UCHL1 is common in primary hepatocellular carcinomas and other digestive tumors. UCHL1 appears to be a functional tumor suppressor involved in the tumorigenesis of hepatocellular carcinomas and other digestive cancers. Ectopic expression of UCHL1 induces apoptosis through intrinsic caspase-dependent pathway. UCHL1 directly interacts with p53 and inhibits p53 protein degradation
-
-
?
additional information
?
-
mono-ubiquitin and ubiquitin dimers may regulate the enzymatic function of UCH-L1 in vivo
-
-
?
additional information
?
-
mono-ubiquitin and ubiquitin dimers may regulate the enzymatic function of UCH-L1 in vivo
-
-
?
additional information
?
-
mono-ubiquitin and ubiquitin dimers may regulate the enzymatic function of UCH-L3 in vivo
-
-
?
additional information
?
-
mono-ubiquitin and ubiquitin dimers may regulate the enzymatic function of UCH-L3 in vivo
-
-
?
additional information
?
-
role for UCH-L1 and ubiquitin modification in podocyte differentiation and injury
-
-
?
additional information
?
-
-
role for UCH-L1 and ubiquitin modification in podocyte differentiation and injury
-
-
?
additional information
?
-
silencing of UCH-L1 in MCF7/Adr cells does not suppress cell growth. Overexpression of UCH-L1 in MCF7 cells induces apoptosis. Apoptosis triggered by UCH-L1 is, at least in part, probably through phosphoinositide 3-kinase/Akt signal pathway
-
-
?
additional information
?
-
-
silencing of UCH-L1 in MCF7/Adr cells does not suppress cell growth. Overexpression of UCH-L1 in MCF7 cells induces apoptosis. Apoptosis triggered by UCH-L1 is, at least in part, probably through phosphoinositide 3-kinase/Akt signal pathway
-
-
?
additional information
?
-
UCH-L1 is a key molecule to regulate tumor-cell invasion by upstream activation of Akt. Expression of UCH-L1 in tumor cells enhances their invasive potential in vitro and in vivo. UCH-L1 changes cell morphology by regulating cell adhesion through Akt-mediated pathway
-
-
?
additional information
?
-
-
UCH-L1 is a player in the signaling pathways that promote the proliferation and invasive capacity of malignant B-cells
-
-
?
additional information
?
-
UCH-L1 is a player in the signaling pathways that promote the proliferation and invasive capacity of malignant B-cells
-
-
?
additional information
?
-
Uch37 activities can be modulated both positively and negatively via dynamic interactions with partner proteins, whereby the proteasome and the hINO80 chromatin-remodeling complex may cooperate to regulate transcription or DNA repair
-
-
?
additional information
?
-
-
Uch37 activities can be modulated both positively and negatively via dynamic interactions with partner proteins, whereby the proteasome and the hINO80 chromatin-remodeling complex may cooperate to regulate transcription or DNA repair
-
-
?
additional information
?
-
-
Cezanne-specific siRNA suppresses Cezanne mRNA and protein by at least 70% in culture cells. It leads to elevated NF-kappaB luciferase reporter gene activity and enhanced expression of IL-8 transcripts in TNFalpha-treated cells. Endogenous Cezanne can attenuate NF-kappaB activation and the induction of pro-inflammatory transcripts in response to TNF receptor signaling. Deubiquitinating activity of Cezanne is essential for NF-kappB suppression. Cezanne can be recruited to activated TNF receptors where it suppresses the build-up of polyubiquitinated RIP1 signal adapter proteins
-
-
?
additional information
?
-
Iso-T shows high preference for the natural Leu-Arg-Gly motif in the P4P2 positions. Only reactivity with norleucine at P4 and lysine at P3 mar the exquisite specificity
-
-
?
additional information
?
-
Iso-T shows high preference for the natural Leu-Arg-Gly motif in the P4P2 positions. Only reactivity with norleucine at P4 and lysine at P3 mar the exquisite specificity
-
-
?
additional information
?
-
Iso-T shows high preference for the natural Leu-Arg-Gly motif in the P4P2 positions. Only reactivity with norleucine at P4 and lysine at P3 mar the exquisite specificity
-
-
?
additional information
?
-
-
Iso-T shows high preference for the natural Leu-Arg-Gly motif in the P4P2 positions. Only reactivity with norleucine at P4 and lysine at P3 mar the exquisite specificity
-
-
?
additional information
?
-
OTU-1 shows similarly to UCH-L3 high specificity in the P2 and P3 positions and less specificity in the P4 position. The P4 position prefers norleucine over leucine, but other bulky amino acids are also accepted, such as tyrosine, tryptophan, phenylalanine or lysine
-
-
?
additional information
?
-
OTU-1 shows similarly to UCH-L3 high specificity in the P2 and P3 positions and less specificity in the P4 position. The P4 position prefers norleucine over leucine, but other bulky amino acids are also accepted, such as tyrosine, tryptophan, phenylalanine or lysine
-
-
?
additional information
?
-
OTU-1 shows similarly to UCH-L3 high specificity in the P2 and P3 positions and less specificity in the P4 position. The P4 position prefers norleucine over leucine, but other bulky amino acids are also accepted, such as tyrosine, tryptophan, phenylalanine or lysine
-
-
?
additional information
?
-
-
OTU-1 shows similarly to UCH-L3 high specificity in the P2 and P3 positions and less specificity in the P4 position. The P4 position prefers norleucine over leucine, but other bulky amino acids are also accepted, such as tyrosine, tryptophan, phenylalanine or lysine
-
-
?
additional information
?
-
UCH-L3 does not show hydrolase activity toward the K48-linked, K63-linked or linear ubiquitin dimer
-
-
?
additional information
?
-
UCH-L3 does not show hydrolase activity toward the K48-linked, K63-linked or linear ubiquitin dimer
-
-
?
additional information
?
-
UCH-L3 shows a preference for leucine at P4, but also a broad tolerance of several other hydrophobic residues at this position. It also shows a surprising selectivity for alanine and valine at P2, in addition to the canonical glycine and high preference at the P3 position and relatively low specificity in the P4 position
-
-
?
additional information
?
-
UCH-L3 shows a preference for leucine at P4, but also a broad tolerance of several other hydrophobic residues at this position. It also shows a surprising selectivity for alanine and valine at P2, in addition to the canonical glycine and high preference at the P3 position and relatively low specificity in the P4 position
-
-
?
additional information
?
-
UCH-L3 shows a preference for leucine at P4, but also a broad tolerance of several other hydrophobic residues at this position. It also shows a surprising selectivity for alanine and valine at P2, in addition to the canonical glycine and high preference at the P3 position and relatively low specificity in the P4 position
-
-
?
additional information
?
-
-
UCH-L3 shows a preference for leucine at P4, but also a broad tolerance of several other hydrophobic residues at this position. It also shows a surprising selectivity for alanine and valine at P2, in addition to the canonical glycine and high preference at the P3 position and relatively low specificity in the P4 position
-
-
?
additional information
?
-
interaction of the ubiquitin carboxyl terminal esterase L1 with alpha2-adrenergic receptors inhibits agonist-mediated p44/42 MAP kinase activation. Uch-L1 binds specifically to the third intracellular loop of alpha2A adrenergic receptor, but also to the respective loops of adrenergic receptors alpha2B, alpha2C, and beta2, overview
-
-
?
additional information
?
-
-
polyubiquitin processing, overview. UCHL1/PGP 9.5 also shows ligase activity when in a dimeric form, overview
-
-
?
additional information
?
-
-
the proteasomal pathway is partially inhibited by UCH-L1M
-
-
?
additional information
?
-
-
UCH L1 forms endogenous complexes with beta-catenin and stabilizes it. The expression and deubiquitinating activity of UCHL1 are required for its own basic promoter activity, therefore UCH L1 up-regulates its expression by activation of the oncogenic beta-catenin/TCF signaling in transformed cells
-
-
?
additional information
?
-
-
UCH-L1 can hydrolyze isopeptide bonds between the C-terminal glycine of Ub and the alpha- or gamma-amino group of lysine on the target proteins. UCH-L3 recognizes and hydrolyzes isopeptide bonds at the C-terminal glycine of either ubiquitin or Nedd8, a ubiquitin-like protein. It shows no ligase activity. UCH-L3 can interact with Lys48-linked ubiquitin dimers to protect it from degradation and meanwhile to inhibit its hydrolase activity, D33 and C95 are essential for the interaction with di-ubiquitin. Neither UCH37 alone nor the UCH37-Adrm1 or UCH37-Adrm1-hRpn2 complexes can hydrolyse Lys48-linked di-ubiquitin efficiently, rather, their incorporation into the 19S complex is required to enable UCH37 to process large ubiquitin protein conjugates such as di-ubiquitin
-
-
?
additional information
?
-
-
UCH-L1 is a deubiquitinating enzyme that catalyses the hydrolysis of polyubiquitin precursors and small ubiquitin adducts
-
-
?
additional information
?
-
UCH-L1 is a deubiquitinating enzyme that catalyses the hydrolysis of polyubiquitin precursors and small ubiquitin adducts
-
-
?
additional information
?
-
-
UCH-L1 is a deubiquitinating enzyme. UCH-L1 increases the synthesis of cystic fibrosis transmembrane conductance regulator, CFTR, but has little effect on the rate of post-translational degradation
-
-
?
additional information
?
-
Phe214 is essential for distal-site substrate binding, and the loss of catalytic activity of the mutant may reflect its reduced affinity toward the substrate. The crystal structure of apo UCHL1 shows that the active-site residues are not aligned in a canonical form, with the nucleophilic cysteine being 7.7 A from the general base histidine, an arrangement consistent with an inactive form of the enzyme
-
-
?
additional information
?
-
-
the apparent catalytic triad of amino acids in UCHL1 is Cys90, His161 and Asp176 in the active site. The region forming a disordered crossover loop limiting access of substrates to the active site is located at positions 140-160, overview
-
-
?
additional information
?
-
UCH-L3 hydrolysis rates for the different engineered substrates are very closely correlated to the thermal stabilities of each attached test protein substrate. The thermal stabilities of the engineered substrates are not altered by fusion to ubiquitin. No substrate: alpha-linked, linear di-ubiquitin
-
-
?
additional information
?
-
-
UCH-L3 hydrolysis rates for the different engineered substrates are very closely correlated to the thermal stabilities of each attached test protein substrate. The thermal stabilities of the engineered substrates are not altered by fusion to ubiquitin. No substrate: alpha-linked, linear di-ubiquitin
-
-
?
additional information
?
-
shRNA decreases mRNA levels and reduces viral genome production. EBV deubiquitinating enzyme BPLF1 interacts with, deubiquitinates, and influences the activity of the Epstein-Barr virus ribonucleotide reductase
-
-
?
additional information
?
-
-
shRNA decreases mRNA levels and reduces viral genome production. EBV deubiquitinating enzyme BPLF1 interacts with, deubiquitinates, and influences the activity of the Epstein-Barr virus ribonucleotide reductase
-
-
?
additional information
?
-
-
the enzyme is necessary for placental and fetal development
-
-
?
additional information
?
-
the enzyme is necessary for placental and fetal development
-
-
?
additional information
?
-
-
core histones and H1 are not cleaved
-
-
?
additional information
?
-
Uch-L1, via the ubiquitin-proteasome system, may play an important role not only in gametogenesis, but also in the gonadal transformation process in the rice field eel
-
-
?
additional information
?
-
Uch-L1 binds to and interacts with monoubiqutin
-
-
?
additional information
?
-
-
isozyme L1 associates and colocalizes with monoubiquitin and elongates ubiquitin half-life, null mutants show a reduced monoubiquitin level in neurons, while overexpression causes an increase in monoubiquitin level, mechanism
-
-
?
additional information
?
-
isozyme L1 associates and colocalizes with monoubiquitin and elongates ubiquitin half-life, null mutants show a reduced monoubiquitin level in neurons, while overexpression causes an increase in monoubiquitin level, mechanism
-
-
?
additional information
?
-
-
the closely related isozymes UCH-L1 and UCH-L3 function as reciprocal modulators of germ cell apoptosis in cryptorchid testis
-
-
?
additional information
?
-
the closely related isozymes UCH-L1 and UCH-L3 function as reciprocal modulators of germ cell apoptosis in cryptorchid testis
-
-
?
additional information
?
-
-
the enzyme is essential for the early apoptotic wave of germinal cells and for sperm quality control during spermatogenesis
-
-
?
additional information
?
-
the enzyme is essential for the early apoptotic wave of germinal cells and for sperm quality control during spermatogenesis
-
-
?
additional information
?
-
-
the enzyme is involved in spermatogenesis
-
-
?
additional information
?
-
the enzyme is involved in spermatogenesis
-
-
?
additional information
?
-
the enzyme is involved in spermatogenesis
-
-
?
additional information
?
-
-
the enzyme plays a role in neural cell apoptosis induced by ischemic retinal injury, e.g. in mice with gracile axonal dystrophy, overview
-
-
?
additional information
?
-
-
UCH-L1 functions in sperm quality control during epididymal maturation
-
-
?
additional information
?
-
UCH-L1 functions in sperm quality control during epididymal maturation
-
-
?
additional information
?
-
-
UCH-L1 regulates the morphology of neural progenitor cells and modulates their differentiation, it mediates and enhances neurogenesis in the embryonic brain
-
-
?
additional information
?
-
UCH-L1 regulates the morphology of neural progenitor cells and modulates their differentiation, it mediates and enhances neurogenesis in the embryonic brain
-
-
?
additional information
?
-
-
Uchl3 is involved in working memory, and plays a role in learning, memory, and synaptic plasticity, uchl3-deficient mice are impaired in acquisition of hippocampus-dependent tasks requiring learning and remembering, but show wild-type long-term memory for context and cued fear conditioning, uchl3-/- mice exhibit wild-type synaptic transmission and plasticity in hippocampal area CA1, overview
-
-
?
additional information
?
-
Uchl3 is involved in working memory, and plays a role in learning, memory, and synaptic plasticity, uchl3-deficient mice are impaired in acquisition of hippocampus-dependent tasks requiring learning and remembering, but show wild-type long-term memory for context and cued fear conditioning, uchl3-/- mice exhibit wild-type synaptic transmission and plasticity in hippocampal area CA1, overview
-
-
?
additional information
?
-
-
the enzyme shows de-ubiquinating activity
-
-
?
additional information
?
-
the enzyme shows de-ubiquinating activity
-
-
?
additional information
?
-
-
affects ubiquitin degradation and alters its metabolism. UCH-L1-mediated increases in ubiquitin levels are a function of UCH L1 affinity for ubiquitin rather than hydrolase activity. The enzyme insures ubiquitin stability within neurons
-
-
?
additional information
?
-
affects ubiquitin degradation and alters its metabolism. UCH-L1-mediated increases in ubiquitin levels are a function of UCH L1 affinity for ubiquitin rather than hydrolase activity. The enzyme insures ubiquitin stability within neurons
-
-
?
additional information
?
-
gracile axonal dystrophy is a syndrome that emanates from dysfunctional ubiquitin carboxyl-terminal hydrolase L-1
-
-
?
additional information
?
-
-
gracile axonal dystrophy is a syndrome that emanates from dysfunctional ubiquitin carboxyl-terminal hydrolase L-1
-
-
?
additional information
?
-
mice overexpressing EF1alpha promoter-driven UCH-L1 in the testis are sterile due to a block during spermatogenesis at an early stage of meiosis. Overexpression of UCH-L1 affects spermatogenesis during meiosis and, in particular, induces apoptosis in primary spermatocytes. UCH-L-1 plays a specific role in the process of mitotic proliferation and differentiation of spermatogonial stem cells during spermatogenesis
-
-
?
additional information
?
-
-
mice overexpressing EF1alpha promoter-driven UCH-L1 in the testis are sterile due to a block during spermatogenesis at an early stage of meiosis. Overexpression of UCH-L1 affects spermatogenesis during meiosis and, in particular, induces apoptosis in primary spermatocytes. UCH-L-1 plays a specific role in the process of mitotic proliferation and differentiation of spermatogonial stem cells during spermatogenesis
-
-
?
additional information
?
-
the enzyme may play a significant role in implantation and placental development, and differentiation of embryonic ectoderm
-
-
?
additional information
?
-
-
the enzyme may play a significant role in implantation and placental development, and differentiation of embryonic ectoderm
-
-
?
additional information
?
-
-
ubiquitin C-terminal hydrolase L3 (Uchl3) is involved in working memory
-
-
?
additional information
?
-
ubiquitin C-terminal hydrolase L3 (Uchl3) is involved in working memory
-
-
?
additional information
?
-
-
ubiquitin hydrolase Uch-L1 rescues beta-amyloid-induced decreases in synaptic function and contextual memory
-
-
?
additional information
?
-
ubiquitin hydrolase Uch-L1 rescues beta-amyloid-induced decreases in synaptic function and contextual memory
-
-
?
additional information
?
-
UCH-L1 may play an important role in neurodegeneration of amyloid lateral sclerosis
-
-
?
additional information
?
-
-
UCH-L1 may play an important role in neurodegeneration of amyloid lateral sclerosis
-
-
?
additional information
?
-
-
UCHL1 is required for normal spermatogenesis and sperm quality control. UCHL1-dependent apoptosis is important in spermatogonial cell and sperm maturation
-
-
?
additional information
?
-
UCHL1 is required for normal spermatogenesis and sperm quality control. UCHL1-dependent apoptosis is important in spermatogonial cell and sperm maturation
-
-
?
additional information
?
-
AT-3 carrying six consecutive glutamines undergoes fragmentation upon incubation at room temperature. Cys14 and His119 are involved in the autolytic activity
-
-
?
additional information
?
-
CYLD negatively regulates RANK signaling by inhibiting TRAF6 ubiquitination and activation of downstream signaling events. CYLD interacts physically with the signaling adaptor p62 and thereby is recruited to TRAF6. CYLD is a crucial negative regulator of osteoclastogenesis and may be involved in the p62/TRAF6 signaling axis
-
-
?
additional information
?
-
is overexpressed in alpha-tocopherol deficient mice
-
-
?
additional information
?
-
mono-ubiquitin and ubiquitin dimers may regulate the enzymatic functions of UCH-L3, in vivo
-
-
?
additional information
?
-
mono-ubiquitin and ubiquitin dimers may regulate the enzymatic functions of UCH-L3, in vivo
-
-
?
additional information
?
-
UCH-L1 expression levels show a time-dependent upregulation in mice ischemia-reperfusion injury condition. Germ cell apoptosis triggers downregulation of UCH-L1 at both mRNA and protein levels, thus, ubiquitination level is impaired. Eevidences of UCH-L1/ubiquitination signaling to the testis ischemia-reperfusion injury in vivo
-
-
?
additional information
?
-
-
UCH-L1 expression levels show a time-dependent upregulation in mice ischemia-reperfusion injury condition. Germ cell apoptosis triggers downregulation of UCH-L1 at both mRNA and protein levels, thus, ubiquitination level is impaired. Eevidences of UCH-L1/ubiquitination signaling to the testis ischemia-reperfusion injury in vivo
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additional information
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UCH-L3 does not function to hydrolyze free ubiquitin dimers
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?
additional information
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UCH-L3 does not function to hydrolyze free ubiquitin dimers
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additional information
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UCH-L1 is a deubiquitinating enzyme, it binds to and stabilize mono-ubiquitin in neurons
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?
additional information
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UCH-L1 is a deubiquitinating enzyme, it binds to and stabilizes mono-ubiquitin in neurons
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additional information
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UCH-L3 is capable of cleaving Ub from the Ub chains in vitro, and UCH-L3 directly hydrolyses polyubiquitinated proteins. Wild-type, but not its hydrolase activity or ubiquitin binding activity deficient, UCH-L3 shows the ability to cleave ubiquitin from polyubiquitinated lysozyme in vitro, which is no substrate of UCH-L1
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additional information
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deubiquitinating as well as deNeddylating activity. Active residues are Cys145, His220 and Asp235
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additional information
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the deubiquitinase readily processes a variety of di-Ub linkages
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-
additional information
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the deubiquitinase readily processes a variety of di-Ub linkages
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additional information
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de novo synthesis of isozyme UCH-L1 in rostral ventrolateral medulla is crucial to survival during mevinphos intoxication, the enzyme is involved in synthesis of ubiquitin which is required for protein targeting in degradation in the ubiquitin-proteasome pathway in neurons, UCH-L1 plays a neuroprotective role
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additional information
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de novo synthesis of isozyme UCH-L1 in rostral ventrolateral medulla is crucial to survival during mevinphos intoxication, the enzyme is involved in synthesis of ubiquitin which is required for protein targeting in degradation in the ubiquitin-proteasome pathway in neurons, UCH-L1 plays a neuroprotective role
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additional information
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overexpression of UCH L1 potentiates ATP-induced currents due to the activation of P2X receptors that are widely distributed in the brain and involved in various biological activities including neurosecretion. UCH-L1 may play an important role in synaptic activity
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additional information
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UCHL1 can act as a ubiquitin hydrolase, and generate free ubiquitin species from precursor ubiquitin polypeptides. Synaptic activation of UCH-L1 is correlated with an increase in the levels of free monomeric ubiquitin
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additional information
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core histones and H1 are not cleaved
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additional information
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enzyme regulation
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additional information
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Bro1-Doa4 interaction involves the C-terminal proline-rich domain of Bro1 and a conserved ELC box motif in Doa4
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additional information
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deubiquitination by Doa4 of cargo proteins and/or some components of the multivesicular body sorting machinery is essential to correct sorting of cargoes into the multivesicular body pathway
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additional information
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H6YUH1 is unable to hydrolyze the linkage of ubiquitin with human growth hormone
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additional information
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PLpro reveals very high specificity in the P4 position, where practically only leucine can be tolerated, and even higher specificity in the P2 position, with only glycine being accepted. However, the P3 position can accommodate a number of different amino acids, with some preference for the hydrophobes leucine and tyrosine, and also for the basic side chains of lysine and arginine, amino acids that possess a substantial hydrophobic character
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additional information
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UCHL3 interacts with peripheral acrosomal plasma membrane proteins
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polyubiquitin + H2O
ubiquitin
type I TGF-beta receptor + H2O
?
UCH37 deubiquitinates and stabilizes type I TGF-beta receptor. Overexpression of UCH37 upregulates TGF-beta-dependent transcription
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ubiquitin-CEP52 + H2O
ubiquitin + CEP52
ubiquitin-CEP80 + H2O
ubiquitin + CEP80
ubiquitin-peptide + H2O
?
ubiquitin-protein + H2O
ubiquitin + protein
ubiquitinyl-Smad2 + H2O
ubiquitin + Smad2
the enzyme de-ubiquitinates both Smad2 and Smad3 and up-regulates their stability
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ubiquitinyl-Smad3 + H2O
ubiquitin + Smad3
the enzyme de-ubiquitinates both Smad2 and Smad3 and up-regulates their stability
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additional information
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polyubiquitin + H2O
ubiquitin
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substrate of UCHL3, no activity with UCHL1/PGP 9.5
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?
polyubiquitin + H2O
ubiquitin
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disassembly of polyubiquitin, terminal step of the proteasome pathway, scheme
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?
polyubiquitin + H2O
ubiquitin
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inhibition by prostaglandins of the J series leads to accumulation of polyubiquitins of MW around 250 kDa
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?
polyubiquitin + H2O
ubiquitin
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substrate of UCHL3, no activity with UCHL1/PGP 9.5
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?
polyubiquitin + H2O
ubiquitin
UCHL5 deubiquitylates the polyubiquitin chain into ubiquitin
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?
polyubiquitin + H2O
ubiquitin
UCHL5 deubiquitylates the polyubiquitin chain into ubiquitin
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?
polyubiquitin + H2O
ubiquitin
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UCHL1/PGP 9.5, overview
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ubiquitin-CEP52 + H2O
ubiquitin + CEP52
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substrate of UCHL1/PGP 9.5, no activity with UCHL3
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?
ubiquitin-CEP52 + H2O
ubiquitin + CEP52
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substrate of UCHL1/PGP 9.5, no activity with UCHL3
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?
ubiquitin-CEP80 + H2O
ubiquitin + CEP80
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substrate of UCHL3 and UCHL1/PGP 9.5
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?
ubiquitin-CEP80 + H2O
ubiquitin + CEP80
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substrate of UCHL3 and UCHL1/PGP 9.5
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?
ubiquitin-peptide + H2O
?
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?
ubiquitin-peptide + H2O
?
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?
ubiquitin-peptide + H2O
?
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?
ubiquitin-peptide + H2O
?
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UCH enzymes may function to regenerate active ubiquitin from adducts with small nuceleophiles
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?
ubiquitin-peptide + H2O
?
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ubiquitin-protein + H2O
ubiquitin + protein
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enzyme is crucial for polarization of the actin cytoskeleton, to segregate germline determinants, to assemble an intact cleavage furrow, for cytokinesis and to maintain osmotic balance and execute actin-dependent processes in the early embryo
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ubiquitin-protein + H2O
ubiquitin + protein
important role in regulation of cell growth
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?
ubiquitin-protein + H2O
ubiquitin + protein
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-
?
ubiquitin-protein + H2O
ubiquitin + protein
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involved in endocytotic pathway of plasma membrane proteins
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?
ubiquitin-protein + H2O
ubiquitin + protein
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Doap4 enzyme form plays a general role in deubiquination of membrane-bound proteins
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?
additional information
?
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uch-L1 may have an important role in the development of neuronal cells in early embryos as well as in the degeneration and disease of neuronal cells in late adult brain. The gene for ubiquitin C-terminal hydrolase L1 is associated with inherited forms of Parkinson's disease
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additional information
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uch-L1 may have an important role in the development of neuronal cells in early embryos as well as in the degeneration and disease of neuronal cells in late adult brain. The gene for ubiquitin C-terminal hydrolase L1 is associated with inherited forms of Parkinson's disease
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additional information
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enzyme inhibits cell proliferation
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additional information
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enzyme inhibits cell proliferation
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?
additional information
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increased activity of neuronal isozyme L1 reduces the risk for Parkinson's disease
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additional information
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increased activity of neuronal isozyme L1 reduces the risk for Parkinson's disease
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?
additional information
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enzyme regulation
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?
additional information
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enzyme regulation
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additional information
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AMSH is a deubiquinating enzyme with functions at the endosome, it opposes the ubiquitin-dependent sorting of receptors to lysosomes, the enzyme influences the degradation of the EGF receptor by association to endosomes, model of the enzyme's physiological function
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?
additional information
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gene uch-L1 is involved in development of Parkinson's disease
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?
additional information
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gene uch-L1 is involved in development of Parkinson's disease
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additional information
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the enzyme is involved in generation of free monomeric ubiquitin, enzyme deficiency leads is involved in accumulation of ubiquitin and alpha-synuclein leading to aggregation in proteins conforming Lewy bodies and Lewy neurites leading to Parkinson's disease and dementia with Lewy bodies, the enzyme is down-regulated in Alzheimer's disease and in Parkinson's disease, comparison of enzyme expression to general protein synthesis and proteasome activity in brain
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additional information
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the full length UCH-L1 is a de-ubiquinating enzyme in brain, and a major target of oxidative damage in Alzheimer's diesease and Parkinson's disease brains, modified by cysteine and methionine oxidation and carbonyl formation
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additional information
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the full length UCH-L1 is a de-ubiquinating enzyme in brain, and a major target of oxidative damage in Alzheimer's diesease and Parkinson's disease brains, modified by cysteine and methionine oxidation and carbonyl formation
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?
additional information
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ubiquitin carboxy-terminal hydrolase L1 activates the P2X receptor leading to potentiation of ATP-induced currents in neurons
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?
additional information
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UCH-L1 is involved in Parkinson's disease
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?
additional information
?
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UCH-L1 is involved in Parkinson's disease
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?
additional information
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UCH-L1 is involved in Parkinson's disease
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?
additional information
?
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UCH-L1 regulates the morphology of neural progenitor cells and modulates their differentiation, it mediates and enhances neurogenesis in the embryonic brain
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?
additional information
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oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase L1 associated with idiopathic Parkinsons and Alzheimers diseases
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?
additional information
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oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase L1 associated with idiopathic Parkinsons and Alzheimers diseases
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?
additional information
?
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UCHL1 is an essential gene in cell survival under normal growth conditions and against oxidative stress
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?
additional information
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UCHL1 is an essential gene in cell survival under normal growth conditions and against oxidative stress
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?
additional information
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UCHL1 is an essential gene to maintain cell homeostasis under normal growth and oxidative stress conditions
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?
additional information
?
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UCHL1 is an essential gene to maintain cell homeostasis under normal growth and oxidative stress conditions
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?
additional information
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UCHL1 is associated with Parkinsons disease
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?
additional information
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Bap1 helps to control cell proliferation by regulating HCF-1 protein levels and by associating with genes involved in the G1-S transition
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?
additional information
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epigenetic inactivation of UCHL1 is common in primary hepatocellular carcinomas and other digestive tumors. UCHL1 appears to be a functional tumor suppressor involved in the tumorigenesis of hepatocellular carcinomas and other digestive cancers. Ectopic expression of UCHL1 induces apoptosis through intrinsic caspase-dependent pathway. UCHL1 directly interacts with p53 and inhibits p53 protein degradation
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?
additional information
?
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mono-ubiquitin and ubiquitin dimers may regulate the enzymatic function of UCH-L1 in vivo
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?
additional information
?
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mono-ubiquitin and ubiquitin dimers may regulate the enzymatic function of UCH-L1 in vivo
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?
additional information
?
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mono-ubiquitin and ubiquitin dimers may regulate the enzymatic function of UCH-L3 in vivo
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?
additional information
?
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mono-ubiquitin and ubiquitin dimers may regulate the enzymatic function of UCH-L3 in vivo
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?
additional information
?
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role for UCH-L1 and ubiquitin modification in podocyte differentiation and injury
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?
additional information
?
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role for UCH-L1 and ubiquitin modification in podocyte differentiation and injury
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?
additional information
?
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silencing of UCH-L1 in MCF7/Adr cells does not suppress cell growth. Overexpression of UCH-L1 in MCF7 cells induces apoptosis. Apoptosis triggered by UCH-L1 is, at least in part, probably through phosphoinositide 3-kinase/Akt signal pathway
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?
additional information
?
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silencing of UCH-L1 in MCF7/Adr cells does not suppress cell growth. Overexpression of UCH-L1 in MCF7 cells induces apoptosis. Apoptosis triggered by UCH-L1 is, at least in part, probably through phosphoinositide 3-kinase/Akt signal pathway
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?
additional information
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UCH-L1 is a key molecule to regulate tumor-cell invasion by upstream activation of Akt. Expression of UCH-L1 in tumor cells enhances their invasive potential in vitro and in vivo. UCH-L1 changes cell morphology by regulating cell adhesion through Akt-mediated pathway
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?
additional information
?
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UCH-L1 is a player in the signaling pathways that promote the proliferation and invasive capacity of malignant B-cells
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?
additional information
?
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UCH-L1 is a player in the signaling pathways that promote the proliferation and invasive capacity of malignant B-cells
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?
additional information
?
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Uch37 activities can be modulated both positively and negatively via dynamic interactions with partner proteins, whereby the proteasome and the hINO80 chromatin-remodeling complex may cooperate to regulate transcription or DNA repair
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?
additional information
?
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Uch37 activities can be modulated both positively and negatively via dynamic interactions with partner proteins, whereby the proteasome and the hINO80 chromatin-remodeling complex may cooperate to regulate transcription or DNA repair
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?
additional information
?
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interaction of the ubiquitin carboxyl terminal esterase L1 with alpha2-adrenergic receptors inhibits agonist-mediated p44/42 MAP kinase activation. Uch-L1 binds specifically to the third intracellular loop of alpha2A adrenergic receptor, but also to the respective loops of adrenergic receptors alpha2B, alpha2C, and beta2, overview
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?
additional information
?
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polyubiquitin processing, overview. UCHL1/PGP 9.5 also shows ligase activity when in a dimeric form, overview
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?
additional information
?
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the proteasomal pathway is partially inhibited by UCH-L1M
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?
additional information
?
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UCH L1 forms endogenous complexes with beta-catenin and stabilizes it. The expression and deubiquitinating activity of UCHL1 are required for its own basic promoter activity, therefore UCH L1 up-regulates its expression by activation of the oncogenic beta-catenin/TCF signaling in transformed cells
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?
additional information
?
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UCH-L1 can hydrolyze isopeptide bonds between the C-terminal glycine of Ub and the alpha- or gamma-amino group of lysine on the target proteins. UCH-L3 recognizes and hydrolyzes isopeptide bonds at the C-terminal glycine of either ubiquitin or Nedd8, a ubiquitin-like protein. It shows no ligase activity. UCH-L3 can interact with Lys48-linked ubiquitin dimers to protect it from degradation and meanwhile to inhibit its hydrolase activity, D33 and C95 are essential for the interaction with di-ubiquitin. Neither UCH37 alone nor the UCH37-Adrm1 or UCH37-Adrm1-hRpn2 complexes can hydrolyse Lys48-linked di-ubiquitin efficiently, rather, their incorporation into the 19S complex is required to enable UCH37 to process large ubiquitin protein conjugates such as di-ubiquitin
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?
additional information
?
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UCH-L1 is a deubiquitinating enzyme that catalyses the hydrolysis of polyubiquitin precursors and small ubiquitin adducts
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?
additional information
?
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UCH-L1 is a deubiquitinating enzyme that catalyses the hydrolysis of polyubiquitin precursors and small ubiquitin adducts
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?
additional information
?
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UCH-L1 is a deubiquitinating enzyme. UCH-L1 increases the synthesis of cystic fibrosis transmembrane conductance regulator, CFTR, but has little effect on the rate of post-translational degradation
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?
additional information
?
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shRNA decreases mRNA levels and reduces viral genome production. EBV deubiquitinating enzyme BPLF1 interacts with, deubiquitinates, and influences the activity of the Epstein-Barr virus ribonucleotide reductase
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?
additional information
?
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shRNA decreases mRNA levels and reduces viral genome production. EBV deubiquitinating enzyme BPLF1 interacts with, deubiquitinates, and influences the activity of the Epstein-Barr virus ribonucleotide reductase
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?
additional information
?
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the enzyme is necessary for placental and fetal development
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?
additional information
?
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the enzyme is necessary for placental and fetal development
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?
additional information
?
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Uch-L1, via the ubiquitin-proteasome system, may play an important role not only in gametogenesis, but also in the gonadal transformation process in the rice field eel
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?
additional information
?
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isozyme L1 associates and colocalizes with monoubiquitin and elongates ubiquitin half-life, null mutants show a reduced monoubiquitin level in neurons, while overexpression causes an increase in monoubiquitin level, mechanism
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?
additional information
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isozyme L1 associates and colocalizes with monoubiquitin and elongates ubiquitin half-life, null mutants show a reduced monoubiquitin level in neurons, while overexpression causes an increase in monoubiquitin level, mechanism
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?
additional information
?
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the closely related isozymes UCH-L1 and UCH-L3 function as reciprocal modulators of germ cell apoptosis in cryptorchid testis
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?
additional information
?
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the closely related isozymes UCH-L1 and UCH-L3 function as reciprocal modulators of germ cell apoptosis in cryptorchid testis
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?
additional information
?
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the enzyme is essential for the early apoptotic wave of germinal cells and for sperm quality control during spermatogenesis
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?
additional information
?
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the enzyme is essential for the early apoptotic wave of germinal cells and for sperm quality control during spermatogenesis
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?
additional information
?
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the enzyme is involved in spermatogenesis
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?
additional information
?
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the enzyme is involved in spermatogenesis
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?
additional information
?
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the enzyme is involved in spermatogenesis
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?
additional information
?
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the enzyme plays a role in neural cell apoptosis induced by ischemic retinal injury, e.g. in mice with gracile axonal dystrophy, overview
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?
additional information
?
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UCH-L1 functions in sperm quality control during epididymal maturation
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?
additional information
?
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UCH-L1 functions in sperm quality control during epididymal maturation
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?
additional information
?
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UCH-L1 regulates the morphology of neural progenitor cells and modulates their differentiation, it mediates and enhances neurogenesis in the embryonic brain
-
-
?
additional information
?
-
UCH-L1 regulates the morphology of neural progenitor cells and modulates their differentiation, it mediates and enhances neurogenesis in the embryonic brain
-
-
?
additional information
?
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Uchl3 is involved in working memory, and plays a role in learning, memory, and synaptic plasticity, uchl3-deficient mice are impaired in acquisition of hippocampus-dependent tasks requiring learning and remembering, but show wild-type long-term memory for context and cued fear conditioning, uchl3-/- mice exhibit wild-type synaptic transmission and plasticity in hippocampal area CA1, overview
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?
additional information
?
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Uchl3 is involved in working memory, and plays a role in learning, memory, and synaptic plasticity, uchl3-deficient mice are impaired in acquisition of hippocampus-dependent tasks requiring learning and remembering, but show wild-type long-term memory for context and cued fear conditioning, uchl3-/- mice exhibit wild-type synaptic transmission and plasticity in hippocampal area CA1, overview
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?
additional information
?
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affects ubiquitin degradation and alters its metabolism. UCH-L1-mediated increases in ubiquitin levels are a function of UCH L1 affinity for ubiquitin rather than hydrolase activity. The enzyme insures ubiquitin stability within neurons
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additional information
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affects ubiquitin degradation and alters its metabolism. UCH-L1-mediated increases in ubiquitin levels are a function of UCH L1 affinity for ubiquitin rather than hydrolase activity. The enzyme insures ubiquitin stability within neurons
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?
additional information
?
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gracile axonal dystrophy is a syndrome that emanates from dysfunctional ubiquitin carboxyl-terminal hydrolase L-1
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?
additional information
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gracile axonal dystrophy is a syndrome that emanates from dysfunctional ubiquitin carboxyl-terminal hydrolase L-1
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?
additional information
?
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mice overexpressing EF1alpha promoter-driven UCH-L1 in the testis are sterile due to a block during spermatogenesis at an early stage of meiosis. Overexpression of UCH-L1 affects spermatogenesis during meiosis and, in particular, induces apoptosis in primary spermatocytes. UCH-L-1 plays a specific role in the process of mitotic proliferation and differentiation of spermatogonial stem cells during spermatogenesis
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?
additional information
?
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mice overexpressing EF1alpha promoter-driven UCH-L1 in the testis are sterile due to a block during spermatogenesis at an early stage of meiosis. Overexpression of UCH-L1 affects spermatogenesis during meiosis and, in particular, induces apoptosis in primary spermatocytes. UCH-L-1 plays a specific role in the process of mitotic proliferation and differentiation of spermatogonial stem cells during spermatogenesis
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?
additional information
?
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the enzyme may play a significant role in implantation and placental development, and differentiation of embryonic ectoderm
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?
additional information
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the enzyme may play a significant role in implantation and placental development, and differentiation of embryonic ectoderm
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?
additional information
?
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ubiquitin C-terminal hydrolase L3 (Uchl3) is involved in working memory
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?
additional information
?
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ubiquitin C-terminal hydrolase L3 (Uchl3) is involved in working memory
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?
additional information
?
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ubiquitin hydrolase Uch-L1 rescues beta-amyloid-induced decreases in synaptic function and contextual memory
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?
additional information
?
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ubiquitin hydrolase Uch-L1 rescues beta-amyloid-induced decreases in synaptic function and contextual memory
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?
additional information
?
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UCH-L1 may play an important role in neurodegeneration of amyloid lateral sclerosis
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?
additional information
?
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UCH-L1 may play an important role in neurodegeneration of amyloid lateral sclerosis
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?
additional information
?
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UCHL1 is required for normal spermatogenesis and sperm quality control. UCHL1-dependent apoptosis is important in spermatogonial cell and sperm maturation
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?
additional information
?
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UCHL1 is required for normal spermatogenesis and sperm quality control. UCHL1-dependent apoptosis is important in spermatogonial cell and sperm maturation
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?
additional information
?
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CYLD negatively regulates RANK signaling by inhibiting TRAF6 ubiquitination and activation of downstream signaling events. CYLD interacts physically with the signaling adaptor p62 and thereby is recruited to TRAF6. CYLD is a crucial negative regulator of osteoclastogenesis and may be involved in the p62/TRAF6 signaling axis
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?
additional information
?
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is overexpressed in alpha-tocopherol deficient mice
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-
?
additional information
?
-
mono-ubiquitin and ubiquitin dimers may regulate the enzymatic functions of UCH-L3, in vivo
-
-
?
additional information
?
-
mono-ubiquitin and ubiquitin dimers may regulate the enzymatic functions of UCH-L3, in vivo
-
-
?
additional information
?
-
UCH-L1 expression levels show a time-dependent upregulation in mice ischemia-reperfusion injury condition. Germ cell apoptosis triggers downregulation of UCH-L1 at both mRNA and protein levels, thus, ubiquitination level is impaired. Eevidences of UCH-L1/ubiquitination signaling to the testis ischemia-reperfusion injury in vivo
-
-
?
additional information
?
-
-
UCH-L1 expression levels show a time-dependent upregulation in mice ischemia-reperfusion injury condition. Germ cell apoptosis triggers downregulation of UCH-L1 at both mRNA and protein levels, thus, ubiquitination level is impaired. Eevidences of UCH-L1/ubiquitination signaling to the testis ischemia-reperfusion injury in vivo
-
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?
additional information
?
-
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UCH-L1 is a deubiquitinating enzyme, it binds to and stabilize mono-ubiquitin in neurons
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?
additional information
?
-
-
UCH-L1 is a deubiquitinating enzyme, it binds to and stabilizes mono-ubiquitin in neurons
-
-
?
additional information
?
-
-
de novo synthesis of isozyme UCH-L1 in rostral ventrolateral medulla is crucial to survival during mevinphos intoxication, the enzyme is involved in synthesis of ubiquitin which is required for protein targeting in degradation in the ubiquitin-proteasome pathway in neurons, UCH-L1 plays a neuroprotective role
-
-
?
additional information
?
-
de novo synthesis of isozyme UCH-L1 in rostral ventrolateral medulla is crucial to survival during mevinphos intoxication, the enzyme is involved in synthesis of ubiquitin which is required for protein targeting in degradation in the ubiquitin-proteasome pathway in neurons, UCH-L1 plays a neuroprotective role
-
-
?
additional information
?
-
-
overexpression of UCH L1 potentiates ATP-induced currents due to the activation of P2X receptors that are widely distributed in the brain and involved in various biological activities including neurosecretion. UCH-L1 may play an important role in synaptic activity
-
-
?
additional information
?
-
-
UCHL1 can act as a ubiquitin hydrolase, and generate free ubiquitin species from precursor ubiquitin polypeptides. Synaptic activation of UCH-L1 is correlated with an increase in the levels of free monomeric ubiquitin
-
-
?
additional information
?
-
-
enzyme regulation
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
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(3E)-1-(3,4-dichlorobenzyl)-4-methoxy-5-phenyl-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0061 mM
(3E)-1-(3,4-dichlorobenzyl)-5-iodo-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.00094 mM; IC50: 0.016 mM
(3E)-1-(3,4-dichlorobenzyl)-5-methoxy-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0029 mM
(3E)-1-{2-bromo-2-[3-(trifluoromethyl)phenyl]ethyl}-5-chloro-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0095 mM
(3E)-3-[(acetyloxy)imino]-1-(3,4-dichlorobenzyl)-2-oxoindoline-5-carbonitrile
-
IC50: 0.012 mM
(3E)-3-[(acetyloxy)imino]-1-(3,4-dichlorobenzyl)-2-oxoindoline-5-carboxamide
-
IC50: 0.0041 mM
(3E)-3-[(acetyloxy)imino]-1-(3,4-dichlorobenzyl)-2-oxoindoline-5-carboxylic acid
-
IC50: 0.05 mM
(3E)-5-(trifluoromethoxy)-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0034 mM
(3E)-5-(trifluoromethoxy)-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
-
IC50: 0.078 mM
(3E)-5-bromo-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.00081 mM
(3E)-5-chloro-1-(2,3-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0027 mM
(3E)-5-chloro-1-(2,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0012 mM
(3E)-5-chloro-1-(2,5-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.00088 mM
(3E)-5-chloro-1-(2-chloro-5-fluorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0065 mM
(3E)-5-chloro-1-(2-naphthylmethyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.014 mM
(3E)-5-chloro-1-(2-phenylethyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.019 mM
(3E)-5-chloro-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0018 mM; IC50: 0.017 mM
(3E)-5-chloro-1-(3,5-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0013 mM
(3E)-5-chloro-1-(3-chloro-4-methoxybenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.021 mM
(3E)-5-chloro-1-(3-methoxybenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.013 mM
(3E)-5-chloro-1-(4-chlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.012 mM
(3E)-5-chloro-1-(4-methoxybenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.052 mM
(3E)-5-chloro-1-[2-(3,4-dichlorophenoxy)ethyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0062 mM
(3E)-5-chloro-1-[2-(3,4-dichlorophenyl)ethyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0013 mM
(3E)-5-chloro-1-[2-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.018 mM
(3E)-5-chloro-1-[2-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
-
IC50: 0.321 mM
(3E)-5-chloro-1-[3-(3,4-dichlorophenyl)propyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.016 mM
(3E)-5-chloro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.006 mM; IC50: 0.036 mM
(3E)-5-chloro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
-
IC50: 0.114 mM
(3E)-5-chloro-1-[4-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.012 mM
(3E)-5-chloro-1-[4-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
-
IC50: 0.013 mM
(3E)-5-chloro-1-{1-[2-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0088 mM
(3E)-5-chloro-1-{1-[2-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-oxime
-
IC50: 0.045 mM
(3E)-5-chloro-1-{1-[3-(trichloromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0034 mM
(3E)-5-chloro-1-{1-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-oxime
-
IC50: 0.022 mM
(3E)-5-chloro-1-{2-ethoxy-2-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.095 mM
(3E)-5-chloro-1-{2-hydroxy-2-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.019 mM
(3E)-5-chloro-1-{2-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0041 mM
(3E)-5-chloro-1-{2-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-oxime
-
IC50: 0.08 mM
(3E)-5-chloro-7-methyl-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.012 mM
(3E)-5-fluoro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0061 mM
(3E)-5-fluoro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
-
IC50: 0.043 mM
(3E)-6-chloro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0058 mM
1-(1,3-benzodioxol-5-ylmethyl)-4-(4-([(4-chlorophenyl)thio]methyl)benzoyl) piperazine
slight inhibition of UCH-L1
1-(3',4'-dihydroxybenzyl)-1,2,3,4-tetrahydroisoquinoline
the enzyme is covalently modified by the endogenous parkinsonism inducing dopamine derivative. 1-(3',4'-dihydroxybenzyl)-1,2,3,4-tetrahydroisoquinoline binds UCH-L1 specifically at Cys152 in vitro. This increases the amount of insoluble UCH-L1 and reduces its hydrolase activity in SH-SY5Y cells
1-benzyl-3-hydroxy-4-(5-methyl-2-furoyl)-5-(3-pyridinyl)-1,5-dihydro-2H-pyrrol-2-one
-
is a competitive inhibitor of UCH-L3, significantly inhibits hydrolysis activity of UCH-L3 by 83.2%
15-deoxy-DELTA12,14-prostaglandin J2
-
modification of UCH-L1 by cyclopentenone prostaglandins causes unfolding and aggregation. A single thiol group on Cys152 reacts with the alpha,beta-unsaturated carbonyl center in the cyclopentenone ring of prostaglandins, resulting in a covalent adduct, spectral analysis, overview
2-([4-(2-furylmethyl)-5-(2-thienylmethyl)-4H-1,2,4-triazol-3-yl]thio)-N-(2-methoxydibenzo[b,d]furan-3-yl)acetamide
-
2-propenal
-
carbonyl modification with 0.1 mM
2-[(5-ethyl-5H-[1,2,4]triazino[5,6-b]indol-3-yl)thio]-N-(4-methyl-2-pyridinyl)acetamide
-
3,5-bis[(4-nitrophenyl)methylidene]-1-prop-2-enoylpiperidin-4-one
i.e. b-AP15, administration of the UCHL5 inhibitor reduces the expression of FN, type I collagen, Smad2/Smad3, and the deposition of collagen in lung tissues in a bleomycin-induced model of pulmonary fibrosis
3-amino-2-(4-methylbenzoyl)-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylaic acid
-
an uncompetitive inhibitor of UCHL1 that binds only to the Michaelis complex and not to free enzyme
3-amino-2-(cyclohexylcarbonyl)-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylic acid
-
-
3-amino-2-keto-7Hthieno[2,3-b]pyridin-6-one derivative
-
-
3-amino-2-[(2-methoxyphenyl)carbonyl]-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylic acid
-
-
3-amino-2-[(4-chlorophenyl)carbonyl]-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylic acid
-
-
3-amino-2-[(4-methylphenyl)carbonyl]-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylic acid
-
-
3-amino-2-[(4-tert-butylphenyl)carbonyl]-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylic acid
-
-
3-amino-2-[(naphthalen-1-yloxy)carbonyl]-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylic acid
-
-
3-amino-2-[(naphthalen-2-yloxy)carbonyl]-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylic acid
-
-
3-amino-6-oxo-2-[[4-(trifluoromethyl)phenyl]carbonyl]-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylic acid
-
-
3-hydroxy-5-(4-methoxyphenyl)-1-(1,3,4-thiadiazol-2-yl)-4-(2-thienylcarbonyl)-1,5-dihydro-2H-pyrrol-2-one
-
significantly inhibits hydrolysis activity of UCH-L3 by 76.5%
3-[4-methyl-5-(([3-(2-thienyl)-1,2,4-oxadiazol-5-yl]methyl)thio)-4H-1,2,4-triazol-3-yl]-1H-indole
-
inhibits hydrolysis activity by 16.2%
4,5,6,7-tetrachloroindan-1,3-dione
-
UCH-L3 inhibition reduces epithelial sodium channel currents, decreases apical membrane epithelial sodium channel expression and increases epithelial sodium channel ubiquitination at the apical surface
4-([benzyl(methyl)amino]sulfonyl)-N-[5-(benzylthio)-1,3,4-thiadiazol-2-yl]benzamide
-
4-hydroxy-2-hexenal
-
carbonyl modification in a dose-dependent manner
4-hydroxy-2-nonenal
-
carbonyl modification with 0.01-0.1 mM leads to decreased ubiquitin binding, and both increased insolubility and interactions with proteins over 30 kDa compared with the wild-type
5-(4-fluorophenyl)-3-hydroxy-4-(5-methyl-2-furoyl)-1-(3-pyridinylmethyl)-1,5-dihydro-2H-pyrrol-2-one
-
significantly inhibits hydrolysis activity of UCH-L3 by 76.8%
5-chloro-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
-
IC50: 0.0018 mM
5-chloro-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-oxime
-
IC50: 0.012 mM
8-[(1H-benzimidazol-2-ylmethyl)sulfanyl]-2,2-dimethyl-5-(morpholin-4-yl)-1,4-dihydro-2H-pyrano[4'',3'':4',5']pyrido[3',2':4,5]thieno[3,2-d]pyrimidine
-
aldehyde product of fatty acid peroxidation
i.e. HNE; modifies isozyme L1 at physiological concentrations of 0.01-0.1 mM and reduces enzyme activity, excess N-acetyl-L-cysteine protects
-
amyloid beta
30% inhibition
-
Antibody
-
anti-UCH antibodies increase the rate of polyspermy during in vitro fertilization by reducing UCH enzymatic activity
-
benzyloxycarbonyl-Val-Ala-Glu(gamma-methoxy) fluoromethylketone
co-crystal structure reveals that the inhibitor binds in the active-site cleft, irreversibly modifying the active-site cysteine
Ca2+
-
59% inhibition at 5 mM
dimethyl sulfoxide
-
catalytic activity decreases slightly with increasing dimethyl sulfoxide concentrations. At 2% (v/v) dimethyl sulfoxide, the proteolytic activity of UCH-L3 is reduced by ca. 5% in comparison to dimethyl sulfoxide-free conditions
DTT
-
erythrocyte isozyme ISOT-S and ISOT-L, inhibition by chelating of Zn2+
epoxysuccinyl-leucylamido-(4-guanidino) butane
reduces UCH-L1 mRNA, protein level and activity. Caspase-mediated apoptosis in epoxysuccinyl-leucylamido-(4-guanidino) butane-treated fibroblasts is reversed by transfection with a UCH-L1 plasmid
isatin O-acyl oximes
-
reversible and competitive inhibition, inhibitory potency and features of the drivatives, specific inhibition of UCH-L1, poor inhibition of UCH-L3, IC50 values, overview
J series prostaglandins
-
inhibition of the enzyme is involved in disruption of the proteasome pathway and leads to apoptosis
-
KCl
-
92% inhibition at 0.2 M
LDN 57 444
UCH-L1 inhibition leads to a time and concentration-dependent formation of membrane protrusions, accompanied by redistribution of alpha-actinin-4 to the membrane. Expression level of alpha-actinin-4 remains stable, whereas the beta-catenin content increases. Inhibition of UCH-L1 does not induce apoptosis
Mg2+
-
61% inhibition at 5 mM
N,N'-(oxydi-4,1-phenylene)dibenzenesulfonamide
slight inhibition of UCH-L1
N,N'-4,4'-biphenyldiylbis(4-ethylbenzenesulfonamide)
strong inhibition of UCH-L1
N-(2-[(6,7-dimethoxy-1-isoquinolinyl)methyl]-4,5-dimethoxyphenyl)-4-(2-oxo-1-pyrrolidinyl)benzenesulfonamide
slight inhibition of UCH-L1
N-(3,6-dichloro-2-pyridinyl)-N'-([(4,6-diphenyl-2-pyrimidinyl)amino]carbonyl)sulfamide
-
N-(4-([(4-ethoxyphenyl)amino]sulfonyl)phenyl)-2-naphthalenesulfonamide
slight inhibition of UCH-L1
N-(4-([(4-methylphenyl)amino]sulfonyl)phenyl)-2-phenyl-2-(phenylthio)acetamide
slight inhibition of UCH-L1
N-[2-(4-benzyl-1-piperazinyl)-2-oxoethyl]-N-(3-methylphenyl)benzenesulfonamide
slight inhibition of UCH-L1
oligomeric Abeta
-
treatment of hippocampal slices produces a deficit in long term potentiation. Effect can be reversed by coadministering a recombinant UCH-L1 protein
-
peptides
-
containing either of the cleavage site sequence found in ubiquitin polymers, but not unrelated peptides
tosyl-L-phenylalanine chloromethyl ketone
inhibits fragmentation of AT-3 carrying six consecutive glutamines
ubiquitin vinyl methyl ester
a ubiquitin-based suicide substrate, binding structure analysis with wild-type and mutant S18Y enzymes, overview
-
ubiquitin vinylmethyl ester
inhibitor forms a covalent adduct with the active site cysteine of the enzyme
-
ubiquitin vinylsulfone
irreversible inhibitor that covalently modifies the active-site cysteines of DUBs
-
iodoacetamide
-
-
iodoacetamide
-
Cys-residue for catalysis
iodoacetamide
-
is a non-competitive inhibitor of UCH-L3
iodoacetamide
-
prevents deubiquitination
LDN-57444
-
a reversible, competitive, active site-directed isatin oxime with consistent preference for UCHL1 over UCHL3 by 28fold
LDN-57444
reversible, competitive, active site-directed isatin oxime, 70% inhibition with 0.005 mM
LDN-57444
-
i.e. 3-(O-acetyloxime), 5-chloro-1-[(2,5-dichlorophenyl)methyl]-1H-indole-2,3-dione
Mn2+
-
-
Mn2+
-
98% inhibition at 5 mM
N-ethylmaleimide
-
UCH-8
RNAi
-
knockdown of UCHL1, leads to short lifespan of animals and earlier accumulation of aging specific lipofucsin with increasing age when compared with the wild-type
-
RNAi
-
knockdown of UCH37, abolishes TGF-beta-dependent transcriptional responses
-
RNAi
knockdown of UCH-L1, inhibits the proliferation of BL cells in suspension and semisolid agar and activates strong LFA-1 dependent homotypic adhesion
-
RNAi
suppressing UCH-L1 expression by RNAi significantly suppresses the invasion in vitro and in vivo, and the activation of Akt and downstream mitogen activates protein kinases c-Jun N-terminal kinases and p38, but not ERK
-
siRNA
-
knockdown of UCHL1 by small interfering RNA results in increased nuclear factor-kappa B activity in A7r5 cells
-
siRNA
inhibits the expression of UCH-L1 in normal control fibroblasts, followed by a remarkable increase of apoptosis both in the presence and in the absence of epoxysuccinyl-leucylamido-(4-guanidino) butane. UCH-L1 siRNA 14311 almost completely inhibits synthesis of UCH-L1 protein in about 70% of cells and reduces the UCH-L1 mRNA level more then 7fold
-
siRNA
stabilization of HCF-1 through depletion of Bap1. Knockdown of Bap1 results in a modest increase in the steady-state levels of HCF-1, which presumably helps to promote the transition from G1 into S-phase
-
siRNA
-
knockdown of UCH-L3 leads to a decrease of epithelial sodium channel currents
-
ubiquitin
-
product inhibition
ubiquitin
-
free ubiquitin acts as a specific, competitive, noncovalent inhibitor
ubiquitin
increasing ubiquitin concentrationin reveals a decrease in the cleavage efficiency, presumably as a result of competition between the second (substrate) ubiquitin molecule and the fluorigenic substrate binding to the enzyme active centre; increasing ubiquitin concentrationin reveals a decrease in the cleavage efficiency, presumably as a result of competition between the second (substrate) ubiquitin molecule and the fluorigenic substrate binding to the enzyme active centre. In the case of OTU-1 full-length ubiquitin does not result in any substantial decrease or increase of the processing of the fluorigenic substrate; increasing ubiquitin concentrationin reveals a decrease in the cleavage efficiency, presumably as a result of competition between the second (substrate) ubiquitin molecule and the fluorigenic substrate binding to the enzyme active centre. In the case of UCH-L3 inhibition of the fluorigenic substrate by elevated concentrations of full-length ubiquitin
ubiquitin
-
submicromolar concentrations activate while higher concentrations inhibit the enzyme, regulatory function, 2-step inhibition mechanism via 2 ubiquitin binding sites extending the active site
Ubiquitin aldehyde
-
-
-
Ubiquitin aldehyde
-
carboxy-terminal aldehyde of ubiquitin
-
Ubiquitin aldehyde
-
UCH-8
-
Ubiquitin aldehyde
inhibition mechanism
-
Ubiquitin aldehyde
-
inhibition in absence of ubiquitin, competitive to ubiquitin
-
Ubiquitin aldehyde
-
specific nonpermeating UCH inhibitor, signficantly increases rates of sperm-zona pellucida penetration and polyspermy during in vitro fertilization by reducing UCH enzymatic activity in motile boar spermatozoa. Ipase-T and ubiquitin aldehyde cancel each other out when added concomitantly to the fertilization medium
-
Ubiquitin aldehyde
-
specific inhibitor for UCH, partly inhibits maturation of ubiquitin precursor derivative in living oocytes
-
ubiquitin-aldehyde
-
-
additional information
-
phenylmethylsulfonyl fluoride does not affect significantly the UCH-enzyme activity
-
additional information
-
not inhibited by phenylmethylsulfonyl fluoride, 1,10-phenanthroline
-
additional information
-
no inhibition by PMSF, EDTA, and o-phenanthroline
-
additional information
-
IC50 above 0.1 mM: (3E)-5-chloro-1-(pyridin-3-ylmethyl)-1H-indole-2,3-dione 3-(O-acetyloxime), (3E)-5-chloro-1-(pyridin-4-ylmethyl)-1H-indole-2,3-dione 3-(O-acetyloxime), 4-({(3E)-3-[(acetyloxy)imino]-5-chloro-2-oxo-2,3-dihydro-1H-indol-1-yl}methyl)benzoic acid
-
additional information
-
the enzyme is inhibited by zinc-chelating agents
-
additional information
-
not inhibited by N1-cyclopropyl-N2-(4-methoxyphenyl)-N2-[(4-methylphenyl)sulfonyl]glycinamide, N-(3-[1-acetyl-5-(2-thienyl)-4,5-dihydro-1H-pyrazol-3-yl]phenyl)ethanesulfonamide, N1-cyclopropyl-N2-[(4-methoxyphenyl)sulfonyl]-N2-(4-methylphenyl)glycinamide, N1-cyclopentyl-N2-(3-methoxyphenyl)-N2-(phenylsulfonyl)glycinamide and 4-(([5-(2-furyl)-4-phenyl-4H-1,2,4-triazol-3-yl]thio)methyl)-1,3-thiazol-2-amine
-
additional information
-
no carbonyl modification with 0.1 mM or 0.5 mM methylglyoxal and 0.1 mM or 0.5 mM malondialdehyde
-
additional information
-
monoubiquitination inhibits ubiquitin binding in vitro and prevents UCH-L1 from regulating free ubiquitin levels in cells involving auto-deubiquitination. Intramolecular deubiquitination, which is dependent on the hydrolytic activity of UCH-L1, regulates the lifetime of monoubiquitination, thereby affecting the cellular level of monoubiquitinated UCH-L1
-
additional information
very high sodium citrate concentrations reveal a decrease in activity; very high sodium citrate concentrations reveal a decrease in activity; very high sodium citrate concentrations reveal a decrease in activity, most dramatic for OTU-1, which is due to enzyme precipitation in the assay
-
additional information
very high sodium citrate concentrations reveal a decrease in activity; very high sodium citrate concentrations reveal a decrease in activity; very high sodium citrate concentrations reveal a decrease in activity, most dramatic for OTU-1, which is due to enzyme precipitation in the assay
-
additional information
very high sodium citrate concentrations reveal a decrease in activity; very high sodium citrate concentrations reveal a decrease in activity; very high sodium citrate concentrations reveal a decrease in activity, most dramatic for OTU-1, which is due to enzyme precipitation in the assay
-
additional information
-
very high sodium citrate concentrations reveal a decrease in activity; very high sodium citrate concentrations reveal a decrease in activity; very high sodium citrate concentrations reveal a decrease in activity, most dramatic for OTU-1, which is due to enzyme precipitation in the assay
-
additional information
in high metastatic potential clones, two isoforms of UCH-L1 are downregulated
-
additional information
-
in high metastatic potential clones, two isoforms of UCH-L1 are downregulated
-
additional information
in vitro, K48-linked ubiquitin dimers pronouncedly inhibit the hydrolase activity of UCH-L3; mono-ubiquitin, a previously identified interacting protein, inhibits the hydrolase activity of UCH-L1
-
additional information
in vitro, K48-linked ubiquitin dimers pronouncedly inhibit the hydrolase activity of UCH-L3; mono-ubiquitin, a previously identified interacting protein, inhibits the hydrolase activity of UCH-L1
-
additional information
kinetics and inhibitor docking study using crystal structure data of PDB code 2ETL, overview. No or poor inhibition by 3-methyl-8-(4-methyl-1-piperazinyl)-7-(3-phenylpropyl)-3,7-dihydro-1Hpurine-2,6-dione, 1-(4-methoxyphenyl)-4-([3-(4-methoxyphenyl)-1,2,4-oxadiazol-5-yl]methyl)piperazine, N1-cyclopropyl-N2-(4-ethoxyphenyl)-N2-[(4-methylphenyl)sulfonyl]glycinamide, N-[6-((2-[(4-chlorophenyl)thio]acetyl)amino)-1,3-benzothiazol-2-yl]butanamide and N-1,3-benzothiazol-2-yl-2-([5-(4-morpholinylmethyl)-4-phenyl-4H-1,2,4-triazol-3-yl]thio)acetamide
-
additional information
-
kinetics and inhibitor docking study using crystal structure data of PDB code 2ETL, overview. No or poor inhibition by 3-methyl-8-(4-methyl-1-piperazinyl)-7-(3-phenylpropyl)-3,7-dihydro-1Hpurine-2,6-dione, 1-(4-methoxyphenyl)-4-([3-(4-methoxyphenyl)-1,2,4-oxadiazol-5-yl]methyl)piperazine, N1-cyclopropyl-N2-(4-ethoxyphenyl)-N2-[(4-methylphenyl)sulfonyl]glycinamide, N-[6-((2-[(4-chlorophenyl)thio]acetyl)amino)-1,3-benzothiazol-2-yl]butanamide and N-1,3-benzothiazol-2-yl-2-([5-(4-morpholinylmethyl)-4-phenyl-4H-1,2,4-triazol-3-yl]thio)acetamide
-
additional information
the binding of SARS-CoV covalent and non-covalent inhibitors to the SARS-CoV-2 papain-like protease and ovarian tumor domain deubiquitinases (OTUB1 and OTUB2) is studied; the binding of SARS-CoV covalent and non-covalent inhibitors to the SARS-CoV-2 papain-like protease and ovarian tumor domain deubiquitinases (OTUB1 and OTUB2) is studied
-
additional information
the binding of SARS-CoV covalent and non-covalent inhibitors to the SARS-CoV-2 papain-like protease and ovarian tumor domain deubiquitinases (OTUB1 and OTUB2) is studied; the binding of SARS-CoV covalent and non-covalent inhibitors to the SARS-CoV-2 papain-like protease and ovarian tumor domain deubiquitinases (OTUB1 and OTUB2) is studied
-
additional information
-
class of 3-amino-2-keto-7H-thieno[2,3-b]pyridin-6-one derivatives are moderately potent UCH-L1 inhibitors. Carboxylate at the 5-position and the 6-pyridinone ring are necessary for inhibitory activity. Inhibitory activity is dependent on the nature of the ketone substituent at the 2-position, with 4-Me-Ph and 2-naphthyl being best. Compounds are uncompetitive inhibitors of UCH-L1, binding only to the Michaelis-complex and not to free enzyme. Active compounds are selective for UCH-L1, exhibiting no inhibition of other cysteine hydrolases or cytotoxicity in serum starved N2A cells. Not inhibited by compound 9, 17, 19, 22, 24, 27, 28, 29, 30, 32 and 33
-
additional information
-
treatment of hippocampal slices with a small-molecule inhibitor of UCH-L1 enzymatic activity produces a deficit in long term potentiation
-
additional information
EDTA, HgCl2 and p-chloro-mecuribenzoate do not inhibit fragmentation of AT-3 carrying six consecutive glutamines
-
additional information
magnitude of induction of uchl1 is lower in asymptomatic, 8-month old, alpha-tocopherol transfer protein deficient mice and in 8-month old mice fed an alpha-tocopherol-depleted diet
-
additional information
-
UCH-L1 is easily affected by redox status
-
additional information
-
very high sodium citrate concentrations reveal a decrease in activity. Full-length ubiquitin does not result in any substantial decrease or increase of the processing of the fluorigenic substrate
-
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0.0061
(3E)-1-(3,4-dichlorobenzyl)-4-methoxy-5-phenyl-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0061 mM
0.00094 - 0.016
(3E)-1-(3,4-dichlorobenzyl)-5-iodo-1H-indole-2,3-dione 3-(O-acetyloxime)
0.0029
(3E)-1-(3,4-dichlorobenzyl)-5-methoxy-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0029 mM
0.0095
(3E)-1-{2-bromo-2-[3-(trifluoromethyl)phenyl]ethyl}-5-chloro-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0095 mM
0.012
(3E)-3-[(acetyloxy)imino]-1-(3,4-dichlorobenzyl)-2-oxoindoline-5-carbonitrile
Homo sapiens
-
IC50: 0.012 mM
0.0041
(3E)-3-[(acetyloxy)imino]-1-(3,4-dichlorobenzyl)-2-oxoindoline-5-carboxamide
Homo sapiens
-
IC50: 0.0041 mM
0.05
(3E)-3-[(acetyloxy)imino]-1-(3,4-dichlorobenzyl)-2-oxoindoline-5-carboxylic acid
Homo sapiens
-
IC50: 0.05 mM
0.0034
(3E)-5-(trifluoromethoxy)-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0034 mM
0.078
(3E)-5-(trifluoromethoxy)-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
Homo sapiens
-
IC50: 0.078 mM
0.00081
(3E)-5-bromo-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.00081 mM
0.0027
(3E)-5-chloro-1-(2,3-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0027 mM
0.0012
(3E)-5-chloro-1-(2,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0012 mM
0.00088
(3E)-5-chloro-1-(2,5-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.00088 mM
0.0065
(3E)-5-chloro-1-(2-chloro-5-fluorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0065 mM
0.014
(3E)-5-chloro-1-(2-naphthylmethyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.014 mM
0.019
(3E)-5-chloro-1-(2-phenylethyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.019 mM
0.0018 - 0.017
(3E)-5-chloro-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
0.0013
(3E)-5-chloro-1-(3,5-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0013 mM
0.021
(3E)-5-chloro-1-(3-chloro-4-methoxybenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.021 mM
0.013
(3E)-5-chloro-1-(3-methoxybenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.013 mM
0.012
(3E)-5-chloro-1-(4-chlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.012 mM
0.052
(3E)-5-chloro-1-(4-methoxybenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.052 mM
0.0062
(3E)-5-chloro-1-[2-(3,4-dichlorophenoxy)ethyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0062 mM
0.0013
(3E)-5-chloro-1-[2-(3,4-dichlorophenyl)ethyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0013 mM
0.018
(3E)-5-chloro-1-[2-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.018 mM
0.321
(3E)-5-chloro-1-[2-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
Homo sapiens
-
IC50: 0.321 mM
0.016
(3E)-5-chloro-1-[3-(3,4-dichlorophenyl)propyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.016 mM
0.006 - 0.036
(3E)-5-chloro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
0.114
(3E)-5-chloro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
Homo sapiens
-
IC50: 0.114 mM
0.012
(3E)-5-chloro-1-[4-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.012 mM
0.013
(3E)-5-chloro-1-[4-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
Homo sapiens
-
IC50: 0.013 mM
0.0088
(3E)-5-chloro-1-{1-[2-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0088 mM
0.045
(3E)-5-chloro-1-{1-[2-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-oxime
Homo sapiens
-
IC50: 0.045 mM
0.0034
(3E)-5-chloro-1-{1-[3-(trichloromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0034 mM
0.022
(3E)-5-chloro-1-{1-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-oxime
Homo sapiens
-
IC50: 0.022 mM
0.095
(3E)-5-chloro-1-{2-ethoxy-2-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.095 mM
0.019
(3E)-5-chloro-1-{2-hydroxy-2-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.019 mM
0.0041
(3E)-5-chloro-1-{2-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0041 mM
0.08
(3E)-5-chloro-1-{2-[3-(trifluoromethyl)phenyl]ethyl}-1H-indole-2,3-dione 3-oxime
Homo sapiens
-
IC50: 0.08 mM
0.012
(3E)-5-chloro-7-methyl-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.012 mM
0.0061
(3E)-5-fluoro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0061 mM
0.043
(3E)-5-fluoro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-oxime
Homo sapiens
-
IC50: 0.043 mM
0.0058
(3E)-6-chloro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0058 mM
0.103
1-benzyl-3-hydroxy-4-(5-methyl-2-furoyl)-5-(3-pyridinyl)-1,5-dihydro-2H-pyrrol-2-one
Homo sapiens
-
-
0.154
3-hydroxy-5-(4-methoxyphenyl)-1-(1,3,4-thiadiazol-2-yl)-4-(2-thienylcarbonyl)-1,5-dihydro-2H-pyrrol-2-one
Homo sapiens
-
-
0.123
5-(4-fluorophenyl)-3-hydroxy-4-(5-methyl-2-furoyl)-1-(3-pyridinylmethyl)-1,5-dihydro-2H-pyrrol-2-one
Homo sapiens
-
-
0.0018
5-chloro-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0018 mM
0.012
5-chloro-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-oxime
Homo sapiens
-
IC50: 0.012 mM
0.015
N,N'-4,4'-biphenyldiylbis(4-ethylbenzenesulfonamide)
Homo sapiens
-
0.00074
ubiquitin
Homo sapiens
-
-
0.1
additional information
Homo sapiens
-
IC50 above 0.1 mM: (3E)-5-chloro-1-(pyridin-3-ylmethyl)-1H-indole-2,3-dione 3-(O-acetyloxime), (3E)-5-chloro-1-(pyridin-4-ylmethyl)-1H-indole-2,3-dione 3-(O-acetyloxime), 4-({(3E)-3-[(acetyloxy)imino]-5-chloro-2-oxo-2,3-dihydro-1H-indol-1-yl}methyl)benzoi
-
0.00094
(3E)-1-(3,4-dichlorobenzyl)-5-iodo-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.00094 mM
0.016
(3E)-1-(3,4-dichlorobenzyl)-5-iodo-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.016 mM
0.0018
(3E)-5-chloro-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.0018 mM
0.017
(3E)-5-chloro-1-(3,4-dichlorobenzyl)-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.017 mM
0.006
(3E)-5-chloro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.006 mM
0.036
(3E)-5-chloro-1-[3-(trifluoromethyl)benzyl]-1H-indole-2,3-dione 3-(O-acetyloxime)
Homo sapiens
-
IC50: 0.036 mM
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brenda
vascular smooth muscle cells. UCH-L1 is up-regulated in injured arteries
brenda
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mRNA and protein expression, expressed in endothelial cells in atherosclerotic lesions from human carotid arteries
brenda
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mRNA and protein expression
brenda
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-
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brenda
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UCH-L1 present in the outer layer cells of the trophectoderm. UCH-L3 present in the inner cells
brenda
the median concentration of UCHL1 in the blood plasma of boys with cryptorchidism, is 5folds higher than in boys with inguinal hernia, whose testicles are located in the scrotum. Significant difference between UCHL1 levels in boys with cryptorchidism up to 2 years old, and above 2 years old. Older boys, whose testicles since birth are located in the inguinal pouch or in the abdominal cavity, have higher concentration of UCHL1 in their blood plasma, than boys from younger group
brenda
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brenda
UCH-L1 is highly expressed
brenda
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brenda
human cervical carcinoma cell line
brenda
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UCHL3 and UCH37 are upregulated in the majority of tumor tissues compared to the adjacent normal tissues. UCH-L1 activity is lower in a significant proportion of the tumors but to a less extent in advanced tumors
brenda
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brenda
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brenda
prefrontal. UCH L1 is 1.1-1.2fold decreased in alcoholics
brenda
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in accordance with the relatively low UCH-L1 activity in tumor biopsies, UCH-L1 is detected only in one out of eight cervical carcinoma lines
brenda
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brenda
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brenda
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brenda
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area 1
brenda
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-
brenda
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brenda
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chinese hamster cell line DON
brenda
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MEFs
brenda
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-
brenda
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brenda
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level of UCH-L3 decreases with age, while the level of UCH-L1 increases with age in wild-type mice
brenda
-
brenda
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-
brenda
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-
brenda
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brenda
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non-small cell lung cancer cell line
brenda
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brenda
isoform UCH-L1 does not partition to the membrane in the cultured cell lines tested
brenda
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-
brenda
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UCH-L3
brenda
UCHL1 expression is low, which is well correlated with its promoter methylation status
brenda
UCHL1 expression is low, which is well correlated with its promoter methylation status
brenda
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lateral
brenda
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a bronchial epithelial cell line, the cells show increased UCH-L1 expression, overview
brenda
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only UCH-L3 is clearly identified in primary keratinocytes. UCH-L1 and UCH-L3 activity is upregulated following HPV E6/E7 immortalization of keratinocytes
brenda
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different cell lines
brenda
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a B lymphoblastoid cell line
brenda
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brenda
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brenda
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brenda
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present in patients with sporadic Parkinson´s disease
brenda
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brenda
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-
brenda
expression level of CYLD is extremely low
brenda
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brenda
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brenda
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MES13 cell line
brenda
-
brenda
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-
brenda
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brenda
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-
brenda
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-
brenda
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-
brenda
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brenda
present in cancerous cells originating from tissues that do not normally express UCH-L1, including pancreatic cancer, colorectal cancer and invasive breast cancer
brenda
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-
brenda
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brenda
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including sensory and motor nerves
brenda
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-
brenda
UCHL1 expression is low, which is well correlated with its promoter methylation status
brenda
CYLD is drastically upregulated during RANKL-induced differentiation of preosteoclasts
brenda
-
brenda
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-
brenda
expression analysis of UCHL! in the renal cell carcinoma system, profiling, overview
brenda
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brenda
de novo synthesis of UCH-L1, leading to an enhanced dissassembly of ubiquitin-protein conjugates in the rostral ventrolateral medulla, is essential to maintenance of the pro-life phase of mevinphos intoxication via prevention of cardiovascular depression, leading to neuroprotection
brenda
human prostate cell line
brenda
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a bronchial epithelial cell line, the cells show increased UCH-L1 expression, overview
brenda
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brenda
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-
brenda
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brenda
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a neuroblastoma cell line
brenda
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brenda
level of UCH-L1 mRNA is significantly reduced in fibroblasts of patients affected with lysosomal storage disorders
brenda
cholinergic neuronal cell line
brenda
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brenda
UCHL1 expression is low, which is well correlated with its promoter methylation status
brenda
-
brenda
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UCHL3 is localized to the acrosomal surface. UCHL1 is absent from the sperm surface
brenda
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brenda
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brenda
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UCHL-1 protein reduced in cases with Lewy body pathology
brenda
strong expression of UCHL1, no expression of UCHL3
brenda
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brenda
human osteosarcoma cell line
brenda
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UCH37 activity is up-regulated in cervical carcinoma biopsies as well as cell lines, while UCH-L1 activity is lower in cervical carcinomas
brenda
human fibroblast cell line
brenda
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brenda
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brenda
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isozyme L1, adult
brenda
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PGP 9.5 represents a ubiquitin carboxy-terminal hydrolase highly, localized in nervous tissue
brenda
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brenda
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-
brenda
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brenda
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UCH-L1
brenda
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accounts for about 2% of soluble protein in brain
brenda
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isozymes ISOT-S and ISOT-L
brenda
isozyme L1, adult
brenda
usp21 gene expression
brenda
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frontal cortex
brenda
frontal cortex of healthy, Alzheimer's disease, and Parkinson's disease brains, 3 isozymes of UCH-L1, UCH-L1 is down-regulated in Alzheimer's diesease and Parkinson's disease brains
brenda
specific for
brenda
oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase L1 associated with idiopathic Parkinsons and Alzheimers diseases
brenda
predominantly neuronal, uniformly expressed throughout brain
brenda
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highly expressed. UCH-L1 expression and protein level are downregulated in the brain of patients with Alzheimer´s disease
brenda
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cortex, UCH-L1M omprises about 30% of total UCH-L1 in diseased and normal human brain
brenda
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high content of UCHL1, distribution in brain tissues, overview
brenda
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UCH-L1 forms 1-5% of total brain protein
brenda
highly expressed in brain
brenda
ubiquitin C-terminal hydrolase L1 is an extremely abundant protein in the brain. It is estimated to make up 1-5% of total neuronal protein
brenda
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high content of UCHL1
brenda
slight expression
brenda
expression of both mRNA and protein
brenda
-
brenda
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-
brenda
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brenda
isozymes L1, specific for neuronal cells, testis and ovary, and L3
brenda
embryonic, UCH-L1 expression in the ventricular zone changes during neurogenesis and gliogenesis, high expression level in cortical plate and ventricular zone, overview
brenda
embryo, expression pattern in the ventricular zone changes between embryonic day 14 and 16, which corresponds to the transition from neurogenesis to gliogenesis. At embryonic day 14, UCH-L1 is highly expressed in the ventricular zone, where neurogenesis actively occurs, whereas its expression is prominent in the cortical plate at embroynic day 16. UCH-L1 is very weakly detected in the ventricular zone at embryonic day 16, which corresponds to the start of gliogenesis. UCH-L1 spatially mediates and enhances neurogenesis in the embryonic brain by regulating progenitor cell morphology
brenda
gracile axonal dystrophy is a syndrome that emanates from dysfunctional ubiquitin carboxyl-terminal hydrolase L-1
brenda
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reduced levels of UCH-L1 mRNA (30%) and protein in a mouse model of Sandhoff disease as compared with their wild-type siblings
brenda
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in mouse brain regions, e.g. cortex, hippocampus, striatum, and midbrain, both UCH-L1M and UCH-L1S occur in varying relative amounts
brenda
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neuron-specific expression of UCH-L1
brenda
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UCH-L1 is one of the most abundant proteins in the mammalian brain
brenda
ubiquitin C-terminal hydrolase L1 is an extremely abundant protein in the brain. It is estimated to make up 1-5% of total neuronal protein
brenda
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neuron-specific expression of UCH-L1
-
brenda
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ubiquitin C-terminal hydrolase is localized especially on the olfactory organ including the olfactory bulb and olfactory epithelium in olfactory rosetta, suggesting the involvement of the protein in chemoreceptive function
brenda
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brenda
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specific expression of UCH-L1
brenda
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brenda
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mRNA expression levels in normal breast tissue are not significantly different between premenopausal and postmenopausal women for both UCH-L1 and UCH-L3
brenda
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UCH-L3 mRNA level is significantly upregulated and UHCL1 mRNA level also show a non-significant increase in breast cancer tissue compared to adjacent normal breast tissue. Both UCH-L1 and UCH-L3 mRNA levels are significantly higher in high histological grade tumors than in low histological grade tumors. UCH-L1 mRNA level in tumors is approximately 10 times higher than that of UCH-L3
brenda
present in cancerous cells originating from tissues that do not normally express UCH-L1, including pancreatic cancer, colorectal cancer and invasive breast cancer
brenda
high expression of UCH-L1
brenda
high expression level of UCH-L1 in caput epididymis
brenda
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brenda
high expression of UCH-L3
brenda
high expression level of UCH-L3 in caudate epididymis
brenda
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brenda
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down-regulation of UCHL-1 mRNA and protein in dementia with Lewy bodies, either in pure forms not associated with Alzheimer disease, and in common forms, with accompanying Alzheimer disease changes, but not in Parkinson disease. UCHL-3 expression reduced in Parkinson disease and dementia with Lewy bodies
brenda
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UCH-L1 levels are specifically increased in cerebrospinal fluid in case of traumatic brain damage, quantitative determination in different samples, overview
brenda
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UCHL1 content determination in benign and malign samples, overview
brenda
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UCH-L1 is significantly elevated in cerebrospinal fluid following controlled cortical impact and middle cerebral artery occlusion, as a model of ischemic stroke, in rats, overview
brenda
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brenda
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colorectal mucosa
brenda
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lymph node metastasis, increased expression
brenda
present in cancerous cells originating from tissues that do not normally express UCH-L1, including pancreatic cancer, colorectal cancer and invasive breast cancer
brenda
recombinant UCH-L1
brenda
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recombinant UCHL1
brenda
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brenda
of chorionic plate and villi
brenda
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brenda
of decidua basalis
brenda
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early stage
brenda
spatiotemporal expression of gene uch-L1 mRNA during embryo development
brenda
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brenda
at 6.5 day of gestation of PGP9.5 is detected at various levels in embryonic ectoderm cells. At 10.5 and 14 day of gestation PGP9.5 is expressed at moderate to strong levels in neurons
brenda
brain, expression pattern in the ventricular zone changes between embryonic day 14 and 16, which corresponds to the transition from neurogenesis to gliogenesis. At embryonic day 14, UCH-L1 is highly expressed in the ventricular zone, where neurogenesis actively occurs, whereas its expression is prominent in the cortical plate at embroynic day 16. UCH-L1 is very weakly detected in the ventricular zone at embryonic day 16, which corresponds to the start of gliogenesis. UCH-L1 spatially mediates and enhances neurogenesis in the embryonic brain by regulating progenitor cell morphology
brenda
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UCH-L1 and UCH-L3 present during all of the embryonic stages. UCH-L1 is essentially constant in all cases, but the level of UCH-L3 is lower in the blastocyst stage. Developing embryos of gad and Uchl3 knockout mice are negative for UCH-L1 and UCH-L3
brenda
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-
brenda
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-
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of mouse hind-paw
brenda
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of mouse hind-paw
brenda
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-
brenda
regiospecific expression of uchl1 and uchl3 in cauda, corpus, and caput, overview
brenda
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UCH-L3 is the predominant deubiquitinating enzyme in endosomal compartments of collecting duct epithelial cells
brenda
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parietal epithelial cells of Bowman's capsules and some tubular epithelia in the kidney
brenda
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-
brenda
renal
brenda
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-
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-
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native isozyme ISOT-S
brenda
accumulated upon growth stimulation of starved human fibroblasts
brenda
weakly expressed in fibroblasts during wound healing
brenda
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embryonic
brenda
-
brenda
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-
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testicular
brenda
low level
brenda
in male gonad epithelium
brenda
-
brenda
usp21 gene expression, high content
brenda
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brenda
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brenda
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-
brenda
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-
-
brenda
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-
brenda
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-
brenda
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epithelium
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epithelium
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usp21 gene expression
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the enzyme is found in tubular and parietal cells of the kidney and is expressed de novo in injured podocytes. Constitutive UCH-L1 expression in tubulointerstitial and glomerular cells
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parietal epithelial cells of Bowman's capsules and some tubular epithelia in the kidney
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usp21 gene expression
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healthy persons, and liver cirrhosis and HCC patients, quantitative USP44 determination, overview
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the enzyme is highly expressed in idiopathic pulmonary fibrosis lungs
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UCHL-1 mRNA and protein expressions reduced in Parkinson disease
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rostral ventrolateral, expression analysis of isozyme UCH-L1 during mevinphos intoxication, overview
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pectoralis
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lung cancer cell line
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non-small cell lung cancer cell line
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at least two populations exist in the embryonic brain, cell culture
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in cultured proliferating NPCs, UCH-L1 is coexpressed with nestin. In differentiating cells, UCH-L1 is highly co-expressed with the early neuronal marker TuJ1
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isoform UCH-L1 does not partition to the membrane in the cultured cell lines tested
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high content of UCHL1. UCHL1/PGP 9.5 is a highly conserved protein present in virtually all neurones and neuroendocrine cells as a major component of soluble cytoplasmic protein
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UCHL1 is neuroendocrine cell-specific. Neuroendocrine gene expression in the large and small airway epithelium, UCHL1 is overexpressed in over 50% of lung cancers, overview
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high content of UCHL1. UCHL1/PGP 9.5 is a highly conserved protein present in virtually all neurones and neuroendocrine cells as a major component of soluble cytoplasmic protein
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high content of UCHL1
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high content of UCHL1
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associated to
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present in patients with Alzheimer´s disease
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isozyme L1
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isozyme L1
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high content of UCHL1. UCHL1/PGP 9.5 is a highly conserved protein present in virtually all neurones and neuroendocrine cells as a major component of soluble cytoplasmic protein
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neuron-specific UCH-L1
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UCH-L1 is abundantly expressed in neuronal cell
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UCH-L1 is present in almost all neurons
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UCHL1 is abundantly and selectively expressed in neurons
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isoform UCHL1 is differently processed in neurons compared with clonal cell lines. In primary cultured neurons, a proportion of UCH-L1M does partition to the membrane, but this does not require farnesylation
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beyond its expression in neurons UCH-L1 has only very limited expression
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the enzyme is highly expressed in neurons
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high content of UCHL1. UCHL1/PGP 9.5 is a highly conserved protein present in virtually all neurones and neuroendocrine cells as a major component of soluble cytoplasmic protein
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high expression of UCH-L1
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neuron-specific isozyme UCH-L1
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the enzyme insures ubiquitin stability within neurons
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high content of UCHL1, distribution in neuron types and cellular compartments, overview
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primary dopaminergic neurons
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UCH-L1 is localized on the inside of the plasma membrane of dorsal root ganglion neurons
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beyond its expression in neurons UCH-L1 has only very limited expression in other healthy tissues but it is highly expressed in several forms of cancer
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UCH-L1 is localized on the inside of the plasma membrane of dorsal root ganglion neurons
-
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interneuron and motor neuron
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high content of UCHL1, distribution in neuron types and cellular compartments, overview
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primary hippocampal neuronal culture
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down regulation of UCHL1 is detected immediately after oxygen-glucose deprivation treatment and its expression is subsequently restored and increased 6 h after oxygen-glucose deprivation treatment as well as during reoxygenation. A lower level of UCHL1 is detected only in apoptotic cells with severe loss of mitochondrial membrane potential. Down-regulation of endogenous UCHL1 by antisense cDNA in mouse N2a neuroblastoma cells increased the cells sensitivity to oxygen-glucose deprivation. This down-regulation of endogenous UCHL1 leads to the accumulation of p27, suggesting that UCHL1 is an essential gene to maintain cell homeostasis under normal growth and oxidative stress conditions
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distribution in cellular compartments, overview
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the olfactory receptor neurones (replaceable) appear to be strongly immunoreactive as do the principal neurones (mitral and mitral/tufted cells), while in the olfactory bulb the replaceable periglomerular and granule cells appear to be non-reactive, distribution in cellular compartments, overview
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subcortical localization of native UCHL1 in bovine oocytes during maturation. Expression of UCHL1 monomer does not change during meiotic maturation of bovine oocytes. Developmental competence is unaffected in parthenogenetic embryos that originated from UCH-L1 inhibitor treated oocytes
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UCH-L1 is associated with the plasma membrane of oocytes
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UCH-L1 and UCH-L3 present in mature oocytes. Oocytes of gad and Uchl3 knockout mice ovaries are negative for UCH-L1 and UCH-L3, respectively
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expression of UCH-L1 in oocytes in prepubertal mouse ovaries, immunohistochemic analysis. Significant decrease in the follicular pool during the period of day 21 to day 28 after birth
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UCHL1 and UCHL3 are present in the oocyte throughout the oestrous cycle in wild-type mice, but appropriately immunoreactivity for UCHL1 is absent from the gad mouse and UCHL3 immunoreactivity is absent from the UCHL3 knock-out mouse, overview
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expression of UCH-L1 in oocytes in prepubertal mouse ovaries, immunohistochemic analysis. Significant decrease in the follicular pool during the period of day 21 to day 28 after birth
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overall level of UCH-L1 increases during maturation
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UCHL1 present in the cortex, UCHL3 is primarly associated with the meiotic spindle of metaphase II ova
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strong cytoplasmic staining of ova in primordial and developing follicles with moderate staining of the theca externa and the corpus luteum
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expression of both mRNA and protein mainly in the developing ovary and slightly in the mature ovary
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slight expression, in degraded ovaries
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isozyme L1, specific for neuronal cells, testis and ovary
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high expression of UCH-L1
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UCH-L1 and UCH-L3 are expressed in ovaries during proestrus, estrus, metestrus, and diestrus. Both proteins are present at all estrous cycle stages in wild-type mice. UCH-L1 is absent from gad ovaries and UCH-L3 from Uchl3 knockout ovaries
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analysis of the ovarian UCH-L1 expression, overview
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analysis of the ovarian UCH-L1 expression, overview
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ubiquitin C-terminal hydrolase localizes especially in pre-vitellogenic oocytes, suggesting that the enzyme activity could be important in oocyte growth
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during the intersex stage, both mRNA and protein is expressed in the male gonad epithelium and degraded ovary
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dominant expression
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usp21 gene expression, high content
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usp21 gene expression
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decidua basalis, the amount of UCH-L1 increases during pregnancy progression
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UCH-L1 is necessary for placental and fetal development in primate placenta
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at 6.5 day of gestation of PGP9.5 is detected at various levels in decidual and primary trophoblast giant cells in the placenta. At 10.5 and 14 day of gestation PGP9.5 is expressed at moderate to strong levels in neurons. At 10.5 and 14 day of gestation PGP9.5 is expressed rarely
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expresses UCH-L1 and expression correlates with the differentiation status. In the cortex of normal biopsies, UCH-L1 is predominantly expressed in distal tubules, macula densa, and nerve fibres. A subset of human glomerulopathies associated with podocyte foot process effacement (membranous nephropathy, SLE class V, FSGS) de novo express UCH-L1 in podocyte cell bodies, nuclei, and processes
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UCHL1 is expressed in podocytes of K256E-ACTN4pod+/UCHL1+/+ mice
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the enzyme is found in tubular and parietal cells of the kidney and is expressed de novo in injured podocytes
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cell culture, expression of UCH-L1 and the regulation of this expression in podocytes, overview
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colorectal mucosa
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UCHL1/PGP 9.5, photoreceptor cells, bipolar cells, and amacrine cells are devoid of staining while the dendrites and axons of both the horizontal cells and the ganglion cells stain strongly
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photoreceptor cells, bipolar cells, and amacrine cells are devoid of staining while the dendrites and axons of both the horizontal cells and the ganglion cells stain strongly
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localization of UCH-L3 in the wild-type retina is altered with age. UCH-L3 is enriched in the photoreceptor inner segment that contains abundant mitochondria. UCH-L1 is expressed in both genotypes in the inner retina, which consists of the inner nuclear layer, inner plexiform layer, and ganglion cell layer
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UCHL1/PGP 9.5, photoreceptor cells, bipolar cells, and amacrine cells are devoid of staining while the dendrites and axons of both the horizontal cells and the ganglion cells stain strongly
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UCH-L1 protein
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UCH-L1 may act during mitotic proliferation of spermatogonial stem cells
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UCHL3
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pectoralis
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usp21 gene expression
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upregulated in skeletal muscles in disease conditions
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UCH-L3 protein
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UCH-L3 may function in the meiotic differentiation of spermatocytes into spermatids
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UCHL3 mainly localized to the round spermatids (acrosomal cap) and elongating spermatids (caudal manchette and acrosome)
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UCH-L3 protein
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UCH-L3 may function in the meiotic differentiation of spermatocytes into spermatids
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spermatogonia in humans can be subdivided into three types, overview
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spermatogonia in monkeys can be subdivided into three types, overview
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UCH-L1 protein
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UCH-L1 may act during mitotic proliferation of spermatogonial stem cells
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UCHL1
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expression level of UCH-L1, high or low, is associated with spermatogonial stem cell self-renewal and differentiation, overview
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UCHL1 is expressed in defective spermatozoa but not in normal spermatozoa
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specific carbonyl level of UCH-L1 is significantly increased in spinal cord of G93A-SOD1 transgenic mice compared to that of nontransgenic mice
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expression of both mRNA and protein in developing germ cells
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dominant expression
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isozyme L1, specific for neuronal cells, testis and ovary
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cryptorchid and healthy
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high expression of UCH-L1
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absence of UCH-L1 causes resistance to cryptorchid-induced testicular germ cell apoptosis. UCH-L1 and UXH-L3 have reciprocal functions, with respect to mediating injury after experimental cryptorchidism
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absence of UCH-L3 promotes germ cell apoptosis after cryptorchid injury. UCH-L1 and UXH-L3 have reciprocal functions, with respect to mediating injury after experimental cryptorchidism
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mice overexpressing EF1alpha promoter-driven UCH-L1 in the testis are sterile due to a block during spermatogenesis at an early stage of meiosis. Overexpression of UCH-L1 affects spermatogenesis during meiosis and, in particular, induces apoptosis in primary spermatocytes. UCH-L-1 plays a specific role in the process of mitotic proliferation and differentiation of spermatogonial stem cells during spermatogenesis
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UCHL1 and UCHL3
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UCH-L1 is exclusively expressed in spermatogonia among male germ cells. In the adult testis, UCH-L1, high or low, is expressed only in a single layer of spermatogonia at the basement membrane
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calf
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isozyme L3
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isozyme L3
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mRNA and protein expression, expressed in vascular smooth muscle cells in atherosclerotic lesions from human carotid arteries
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additional information
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PA700 regulatory complex of 26S proteasome
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additional information
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tissue distribution and immunohistochemic analysis, overview
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additional information
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tissue-specific regulation of uhc-L1 gene expression, analysis, overview
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additional information
tissue-specific regulation of uhc-L1 gene expression, analysis, overview
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additional information
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no expression of UCH-L1 in healthy lung tissue
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additional information
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proteomic analysis
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additional information
proteomic analysis
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additional information
the enzyme is absent in tissues other than brain
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additional information
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the enzyme is absent in tissues other than brain
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additional information
HMVEC cells from newborn foreskins
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additional information
is highly abundant in the PA700 complex
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additional information
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the human papilloma virus-negative C33A cell line is the only cell line lacking detectable UCH-L3 activity
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additional information
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UCHL1 is consistently up-regulated in airway epithelium of smokers compared with nonsmokers. UCHL1 expression is evident only in neuroendocrine cells of the airway epithelium in nonsmokers, whereas it is expressed in neuroendocrine cells and in ciliated epithelial cells in smokers
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additional information
UCHL1 is downregulated in the frontal cortex of frontotemporal dementia and parkinsonism linked to chromosome 17
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additional information
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UCHL1 is downregulated in the frontal cortex of frontotemporal dementia and parkinsonism linked to chromosome 17
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additional information
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vasculature
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additional information
four UCH-L1 isoforms in SN12C clones
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additional information
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four UCH-L1 isoforms in SN12C clones
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additional information
normal kidneys express no UCH-L1 and little ubiquitin. Decrease of expression with differentiation. Minimal change glomerulonephritis demonstrates minimal UCH-L1 and ubiquitin expression with intact alpha-actinin-4 but internalized nephrin. Glomerular kidney diseases typically not associated with foot process effacement (SLE class IV, ANCA+ necrotizing GN, amyloidosis, IgA nephritis) express intermediate to no UCH-L1 and ubiquitin
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additional information
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normal kidneys express no UCH-L1 and little ubiquitin. Decrease of expression with differentiation. Minimal change glomerulonephritis demonstrates minimal UCH-L1 and ubiquitin expression with intact alpha-actinin-4 but internalized nephrin. Glomerular kidney diseases typically not associated with foot process effacement (SLE class IV, ANCA+ necrotizing GN, amyloidosis, IgA nephritis) express intermediate to no UCH-L1 and ubiquitin
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additional information
present in HuH-4 cells. Cancer cell lines HCT-116, EC-109, Hep-3B, HuH-1, HuH-6, Mahlavu, SNU-387 and SNU-449 have silenced UCHL1, which is well correlated with its promoter methylation status
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additional information
UCH-L1 is highly expressed in H157 cells, having high invasive potential. In Akt-negative mutants, overexpression of UCH-L1 does not affect the invasion and migration capability of H157 cells
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additional information
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the deubiquitinating enzyme, ubiquitin C-terminal hydrolase-L1, is highly expressed in cystic fibrosis airway epithelial cells in vitro and in vivo
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additional information
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UCH-L1 is enriched in the central nervous system
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additional information
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UCH-L1 is present in neurofibrillary tangles or Lewy bodies
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additional information
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UCH-L1 levels are high in various types of malignancies: acute lymphoblastic leukemia, non-small cell lung cancer, neuroblastoma, pancreatic, prostate, medullary thyroid, esophageal, colorectal and renal carcinomas
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additional information
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UCHL1/PGP 9.5 is present prominently in brain, in addition to its neuronal localization, UCHL1/PGP 9.5 is also present in cells of the diffuse neuroendocrine system, traces of the protein are also seen in large intestine, kidney, ovary, and testis. Tissue distribution and immunohistochemic analysis, overview. Enzyme activity in the diffuse neuroendocrine system, e.g. in gastroenteropancreatic system, prostate, pulmonary neuroendocrine system, and cerebral cortex, detailed overview
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additional information
UCHL5 is constitutively expressed in several tissues, expression analysis, overview
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additional information
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UCHL5 is constitutively expressed in several tissues, expression analysis, overview
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additional information
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UCHL5 is constitutively expressed in several tissues, expression analysis, overview
-
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additional information
Uch-L1 is upregulated during gonadal transformation, especially from the beginning of the intersex stage onwards
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additional information
no expression in heart, liver, kidney, or spleen. Uch-L1 is upregulated during gonadal transformation from female to male, overview
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additional information
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no isozyme L1 expression in embryonic fibroblasts
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additional information
no isozyme L1 expression in embryonic fibroblasts
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additional information
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isozyme L3 is universally expressed in all tissues
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additional information
isozyme L3 is universally expressed in all tissues
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additional information
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expression pattern of UCH isozymes in Sertoli cells, spermatids, spermatocytes, and spermatogonia, overview
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additional information
expression pattern of UCH isozymes in Sertoli cells, spermatids, spermatocytes, and spermatogonia, overview
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additional information
expression pattern of UCH isozymes in Sertoli cells, spermatids, spermatocytes, and spermatogonia, overview
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additional information
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quantitative testicular expression analysis of UCHL1
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additional information
quantitative testicular expression analysis of UCHL1
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additional information
3T3 cell
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additional information
3T3 cell
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additional information
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absence of UCHL1 in the gracile axonal dystrophy mouse, which results in neurodegeneration
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additional information
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UCH-L1 is upregulated and more abundantly expressed in germ line stem cells than in embryonic stem cells
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additional information
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increased expression and activity of UCH L1 in EBV-immortalized cell lines
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additional information
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tissue distribution and immunohistochemic analysis, overview
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additional information
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UCH-L1 is exclusively expressed in brain and testis
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additional information
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UCH-L1 is exclusively expressed in brain and testis
-
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additional information
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UCH-L1 is upregulated and more abundantly expressed in germ line stem cells than in embryonic stem cells
-
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additional information
FR3T3 cell
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additional information
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immunohistochemic analysis, overview
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additional information
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tissue distribution and immunohistochemic analysis, overview
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additional information
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UCH-L1 expression in podocytes is significantly higher in acute proliferative glomerulonephritis, lupus nephritis, membranous glomerulonephritis, and IgA nephropathy than that in focal segmental glomerulosclerosis, minimal change disease, minor abnormality and normal kidney tissues, overview
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additional information
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in pigs, gonocytes and spermatogonia expressing UCH-L1 include the population expressing PLZF, a known determinant of undifferentiated spermatogonial stem cells, asymmetric segregation of UCH-L1 and PLZF in spermatogonia in vivo and in vitro, overview
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malfunction
-
altered UCH-L1 activity leads to deleterious effects on synapse structure and function. Inhibition of UCH-L1 activity affects synaptic protein clusters
malfunction
-
deficiency of UCH-L1 leads to vulnerability to lipid peroxidation both in vivo and in vitro
malfunction
-
elevation in UCH-L1 in cystic fibrosis cells represents a cellular adaptation to counterbalance excessive proteasomal degradation
malfunction
-
human UCHL1 gene and neurological diseases, wild-type and mutants I93M and S18Y, mutation I93M is proposed as a familial Parkinsons disease mutation, PARK5, detailed overview
malfunction
-
in the absence of UCH-L1, synaptic transmission at the neuromuscular junctions is markedly impaired. Loss of normal UCH-L1 activity may result in neurodegeneration in the peripheral nervous system
malfunction
-
increased oxidative carbonyl modification of UCH-L1 causes dysfunction of UCH-L1 and finally induces neuron death
malfunction
-
increased UCH-L1 protein, together with the corresponding changes of Jab1, is detected in morphologically abnormal oocytes of prepubertal ovaries
malfunction
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the deubiquitinating enzyme USP44 is a critical regulator of the spindle checkpoint, dysregulation of the spindle checkpoint can contribute to birth defects and tumorigenesis
malfunction
-
the enzyme expression is increased in lymph node metastasis associated with poor prognosis in colorectal cancer
malfunction
the hydrolase activity of UCH-L1 is implicated in Alzheimer's disease and cancer invasion
malfunction
-
ubiquitin thiolesterase polymorphisms have synergic effect on the risk of Parkinson's disease among Taiwanese
malfunction
ubiquitination by UCH-L1 is involved in ischemia-reperfusion stress
malfunction
-
UCH enzymes and human malignancies are closely correlated with roles of UCH enzymes in oncogenesis, UCH-L1 enhances tumor cell invasion and migration capability via the Akt-mediated pathway, overview. Dysfunction of UCH-L1 hydrolase activity can lead to an accumulation of alpha-synuclein and neurofibrillary tangles, which links to Parkinson's disease and Alzheimer's disease, respectively. Increased levels of both UCH-L1 and UCH-L3 mRNA are associated with early tumor recurrence of invasive breast cancer and poor prognosis. UCH37 activity is up-regulated in cervical carcinoma biopsies as well as cell lines. UCH-L1 levels are high in various types of malignancies: acute lymphoblastic leukemia, non-small cell lung cancer, neuroblastoma, pancreatic, prostate, medullary thyroid, esophageal, colorectal and renal carcinomas, although lowered in cervical carcinomas
malfunction
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UCH L1 is expressed in a number of malignancies, it might be involved in oncogenic processes. UCH L1 suppression induces G0/G1 arrest and apoptosis
malfunction
Uch-L1 is associated with Parkinson's disease, as alpha2-adrenergic receptor interacting protein. alpha2-Adrenergic receptor agonist-mediated activation of p44/42MAP kinase is drastically decreased in the presence of Uch-L1. Stimulation of recombinantly UCH-L1 expressing HEK-293 cells prior lysis with norepinephrine, yohimbine, phentolamine or moxonidine does also not significantly affect the interaction, as well as co-transfection of arrestin-3 or spinophilin-(Phe151-Lys446)
malfunction
UCH-L1 is highly expressed in Burkitt's lymphoma and is up-regulated upon infection of B lymphocytes with Epstein-Barr virus, EBV. Selective up-regulation of the ubiquitin C-terminal hydrolase UCH-L1 in a variety of metastatic tumours contributes to the malignant phenotype
malfunction
-
UCH-L1 is implicated in Parkinsons disease and is present in neurofibrillary tangles or Lewy bodies
malfunction
UCH-L1 is up-regulated in injured arteries, via posttranscriptional regulation, and local gene delivery of UCH-L1 inhibited vascular lesion formation with suppression of inflammatory responses in vasculature. ERK activation also contributes to the growth inhibitory effect of UCH-L1 in TNFalpha-inflamed vascular smooth muscle cells
malfunction
-
UCH-L1 levels are increased in cerebrospinal fluid in case of traumatic brain damage correlated with a negative survival prognosis, overview
malfunction
-
UCHL1 is overexpressed in over 50% of lung cancers, its overexpression in chronic smokers may represent an early event in the complex transformation from normal epithelium to overt malignancy
malfunction
-
UCHL1 overexpression is associated with tumor progression and an altered von Hippel Lindau gene expression in renal cell carcinoma
malfunction
-
10-week-old K256E-ACTN4pod+/UCHL1-/- mice exhibit reduced albuminuria, glomerulosclerosis, foot process effacement, glomerular basement membrane thickening, glomerular and tubular cell apoptosis, and ameliorated renal pathology. Observations coincide with decreased polyubiquitinated protein levels and increased K256E-alpha-actinin-4 levels in K256E-ACTN4pod+/UCHL1-/-mice kidneys, suggesting impaired proteolysis of K256E-alpha-actinin-4
malfunction
gain- and loss of-function studies reveals that UCH-L1 enhances proliferation of multiple cell types
malfunction
RNA interference of UCH-L1 reduces the growth of human xenograft tumors in mice
malfunction
gene knockdown of UCHL1 by siRNA results in a significant decrease in cell proliferation but marked acceleration of cell differentiation and myotube formation. UCHL1 gene knockdown upregulates myogenic factors myoD and Myogenin (MyoG)
malfunction
UCH-L1 dysfunction is implicated in neurodegenerative disease
malfunction
UCH-L1 dysfunction is implicated in neurodegenerative disease
malfunction
UCH-L1-deficient mice develop proteinuria, without gross changes in glomerular morphology. Tubular cells, endothelial cells, and podocytes show signs of stress with an accumulation of oxidative modified and polyubiquitinated proteins. Mechanistically, abnormal protein accumulation results from an altered proteasome abundance leading to decreased proteasomal activity. UCH-L1-deficient mice exhibit an exacerbated course of disease with increased tubulointerstitial and glomerular damage, acute renal failure, and death, the latter most likely a result of general neurologic impairment
malfunction
-
deficiency of UCH-L1 leads to vulnerability to lipid peroxidation both in vivo and in vitro
-
malfunction
-
increased UCH-L1 protein, together with the corresponding changes of Jab1, is detected in morphologically abnormal oocytes of prepubertal ovaries
-
metabolism
-
the proteasomal pathway is partially inhibited by UCH-L1M
metabolism
-
ubiquitin carboxyl-terminal hydrolase L1 is a member of the ubiquitin proteasome pathway
metabolism
-
UCH-L1 in cell signaling, detailed overview
metabolism
-
UCH-L1 in cell signaling, detailed overview
metabolism
-
UCHL1 gene regulation, overview
metabolism
-
USP44 is a member of the ubiquitin proteasome pathway controlling intracellular protein degradation, functioning to maintain ubiquitin balance by associating with ubiquitin and by releasing ubiquitin from tandemly conjugated ubiquitin monomers and small adducts or unfolded proteins
metabolism
overexpression of ubiquitin carboxyl terminal hydrolase-L1 enhances multidrug resistance and invasion/metastasis in breast cancer by sctivating the MAPK/Erk signaling pathway
metabolism
the enzyme de-ubiquitinates both ubiquitinyl-Smad2 and ubiquitinyl-Smad3 and up-regulates their stability. It mitigates TGFbeta-1 signaling by stabilizing Smad2/Smad3. Inhibition or down-regulation of ubiquitin carboxyl-terminal hydrolase-L5 reduces Smad2/Smad3 levels and TGFbeta-1-induces the expression of fibronectin and alpha-SMA in human lung fibroblast
metabolism
the enzyme is required for regulated protein degradation through the ubiquitin proteasome system in kidney
metabolism
UCH-L1 associates with lipid rafts as with other Parkinson's disease-associated gene products. In addition, UCH-L1 regulates lipid raft-dependent endocytosis and it is not dependent on the expression and degradation of caveolin-1 or flotillin-1. UCH-L1 regulates cell-to-cell transmission of alpha-synuclein. The study provides evidence that many Parkinson's disease-associated gene products share common signaling pathways to explain the pathogenesis of Parkinson's disease
physiological function
-
role of UCH-L1 in synaptic function in the brain, overview
physiological function
-
UCH L1 up-regulates beta-catenin/TCF signaling. UCH L1 forms endogenous complexes with beta-catenin, stabilizes it and up-regulates beta-catenin/TCF-dependent transcription. The deubiquitinating activity of UCH L1 is required for TCF4 transcriptional activity, overview
physiological function
UCH-L1 appears to be a multi-functional protein and exerts cell type and/or tissue specific actions
physiological function
-
UCH-L1 is a deubiquitinating enzyme, it binds to and stabilize mono-ubiquitin in neurons
physiological function
-
UCH-L1 is a deubiquitinating enzyme, it binds to and stabilizes mono-ubiquitin in neurons
physiological function
-
UCH-L1 is a deubiquitinating enzyme. UCH-L1 is a deubiquitinating enzyme. UCH-L1 increases the synthesis of cystic fibrosis transmembrane conductance, and endogenous UCH-L1 expression is positively correlated with CFTR biogenesis
physiological function
-
UCH-L1 is a functional protein that may play a significant role in cell migration
physiological function
UCH-L1 is a player in the signalling pathways that promote the proliferation and invasive capacity of malignant B cells
physiological function
Uch-L1 is involved in controling alpha2-adrenergic receptor receptor function and trafficking, it binds preferentially to the alpha2A-adrenergic receptor subtype and only with less affinity to alpha2B-adrenergic receptor and alpha2C-adrenergic receptor, specific interaction in vivo, mechanism, overview
physiological function
-
UCH-L1 is one of the major de-ubiquitinating enzymes in the brain which controls ubiquitin homeostasis. UCH-L1 function is required for synaptic plasticity and is itself regulated by synaptic activity. UCH-L1 activity is required for NMDA-induced up-regulation of free monomeric ubiquitin. UCH-L1 can also bind to ubiquitin and act as a ubiquitin stabilizer to prevent its degradation by lysosomes. UCH-L1 regulates spine morphology and density
physiological function
-
UCH-L1 is responsible for hydrolyzing carboxyl terminal esters and amides of ubiquitin. Additionally, it possesses ubiquitin ligase activity and functions as a mono-ubiquitin stabilizer, which is independent of enzymatic activity, and is also involved in the co-translational processing of pro-ubiquitin and ribosomal proteins translated as ubiquitin fusions. UCH-L3 is a kind of ubiquitin-protein hydrolase involved in the processing of both ubiquitin precursors and ubiquitinated substrates, generating free monomeric ubiquitin. UCH37, different from other UCH members, is responsible for the Ub isopeptidase activity in the 19S proteasome regulatory complex, overview. UCH-L3 shows deneddylating activity, the only target proteins for neddylation are cullins, which are involved in cell-cycle control, therefore UCH-L3 might function as a cell-cycle regulator
physiological function
-
UCH-L1 mediates maintenance of the temporal integrity and persistence of cyclic AMP response element binding protein, CREB, phosphorylation in the brain
physiological function
-
UCH-L1 plays a crucial role in regulating certain signalings. UCH-L1 forms endogenous complexes with beta-catenin, stabilizes it and up-regulates beta-catenin/TCF/Lef-dependent transcription. Reciprocally, as indicated, beta-catenin/TCF/Lef signaling up-regulates the expression of endogenous UCH-L1 mRNA and protein. UCH-L1 is responsible for hydrolyzing carboxyl terminal esters and amides of Ub. Additionally, it possesses ubiquitin ligase activity and functions as a mono-ubiquitin stabilizer, which is independent of enzymatic activity, and is also involved in the co-translational processing of pro-ubiquitin and ribosomal proteins translated as ubiquitin fusions. UCH-L3 is a kind of ubiquitin-protein hydrolase involved in the processing of both ubiquitin precursors and ubiquitinated substrates, generating free monomeric ubiquitin. UCH37, different from other UCH members, is responsible for the Ub isopeptidase activity in the 19S proteasome regulatory complex, overview. Upregulation of TGF-beta signaling by UCH37
physiological function
UCH-L1 plays an important role in maintaining the intracellular levels of the ubiquitin
physiological function
Uch-L1 plays an important role in the maintenance of intracellular monoubiquitin levels by generating ubiquitin through the hydrolysis of polyubiquitinated proteins, and regulates the ubiquitin pathway. It is important in gametogenesis and gonadal transformation
physiological function
-
UCH-L3 functions as a de-ubiquitinating enzyme in vivo. The polyubiquitinated protein accumulation in Uchl3-/- embryonic fibroblasts is attenuated by the exogenous expression of wild-type, but not hydrolase activity deficient UCH-L3
physiological function
-
UCH-L3 promotes insulin signaling and adipogenesis
physiological function
-
UCHL1 is a component of the ubiquitin system, and the UCH-L1-dependent apoptosis is important for spermatogenesis. UCH-L1 plays an important role, possibly in association with Jab1 and p27Kip1, in selective elimination of abnormal oocytes during mouse prepubertal development
physiological function
-
UCHL1 is involved in the degradation of unwanted, misfolded, or damaged proteins within the cell
physiological function
-
UCHL1 promotes disassembly of polyubiquitin chains during meiotic maturation. Conversely, UCHL1 regulates formation of polyubiquitin chains in bovine oocytes
physiological function
-
UCHL1/PGP 9.5 is important in the ubiquitin system, and functions of UCHL1/PGP 9.5 in neurones, detailed overview
physiological function
-
UCHL1/PGP 9.5 is important in the ubiquitin system, detailed overview
physiological function
-
UCHL1/PGP 9.5 is important in the ubiquitin system, detailed overview
physiological function
-
UCHL1/PGP 9.5 is important in the ubiquitin system, detailed overview. UCHL1/PGP 9.5 might be involved in blocking polyspermy, particularly at the plasma membrane
physiological function
UCHL5 is involved in the ubiquitin-proteasome pathway
physiological function
-
USP44 is a member of the ubiquitin proteasome pathway controlling intracellular protein degradation, functioning to maintain ubiquitin balance by associating with ubiquitin and by releasing ubiquitin from tandemly conjugated ubiquitin monomers and small adducts or unfolded proteins. Deubiquitinating enzyme USP44 is a critical regulator of the spindle checkpoint
physiological function
-
both biomarkers UCH-L1 and glial fibrillary acidic protein(GFAP) discriminate between traumatic brain injury (TBI) patients with intracranial lesions on CT scan from those without such lesions. GFAP measures are significantly more sensitive and specific than UCH-L1. The addition of UCH-L1 values marginally improved upon GFAP alone in predicting dichotomized Glasgow Outcome Scale Extended (GOS-E) at 3 months after injury
physiological function
-
compared with controls, CO-poisoned patients have significantly elevated serum levels of UCH-L1 at each time point after poisoning. There are significantly higher levels of UCH-L1 in CO-poisoned patients with a lower Glasgow coma scale (GCS) score as well as in those with a poor 6-month outcome dichotomized Glasgow outcome scale (GOS)
physiological function
expression of isoform UCHL1 is elevated in osteosarcoma compared with normal bone tissue. UCHL1 expression level is correlated with tumor maximum diameter, high rate of lung metastases and short survival time. Knockdown of UCHL1 in osteosarcoma cell MG-63 inhibits cell proliferation and significantly increases cell population in the G1 phase. Cyclins promoting G1/S phase transition are reduced after UCHL1 knockdown, including cell cycle regulator cyclin D1, cyclin E1 and CDK6. Inhibition of UCHL1 in MG-63 cells dramatically induces cell apoptosis. Downregulation of UCHL1 in MG-63 significantly inhibits cell invasion. There is a positive correlation between UCHL1 expression level and the Akt and ERK phosphorylation status
physiological function
-
high glucose increases the TGF-betaR1 protein expression via the PI3K-UCHL5 pathway in mesangial cells
physiological function
isoform UCHL1 physically interacts with high affinity choline transporter CHT, which is a key protein regulating Ach re-synthesis. Reduction of UCHL1 by siRNA gene knockdown significantly increases polyubiquitinated CHT and decreased native CHT protein level, but does not affect CHT mRNA expression. Gene knockdown of UCHL1 significantly reduces cytosolic CHT but has no significant effect on membrane CHT level
physiological function
melanoma cells show a a widespread loss or reduced expression of ubiquitin C-terminal hydrolase UCHL1, which is directly correlated with promoter DNA hypermethylation. The subset of melanoma cells, which still express UCHL1, shows altered growth properties and tolerances against reactive oxygen species as compared to UCHL1-negative cells
physiological function
-
over-expression of dUCH in the eye imaginal discs induces a rough eye phenotype in the adult, at least partly resulting from the induction of caspase-dependent apoptosis followed by compensatory proliferation. The over-expression of dUCH specifically impairs R7 photoreceptor cell differentiation with a reduction in activated extracellular-signal regulated kinase signals. The dUCH-induced rough eye phenotype is rescued by co-expression of the sevenless gene or the Draf gene, a downstream component of the mitogen-activated protein kinase (MAPK) cascade
physiological function
-
RNAi-mediated knockdown of the ubiquitin hydrolase, USP22, results in 2fold increase in monoubiquitinated histone H2B, and 2fold decrease in transcriptional elongation at IRF1. USP22 depletion diminishes 3'-end cleavage/polyadenylation by 2- to 3fold. The polyadenylation factor CPSF73 is not effectively recruited, and serine 2 phosphorylation of the C-terminal domain of RNA polymerase II is also disrupted. Results suggest that ubiquitinated histone H2B helps recruit polyadenylation factors to STAT1-activated genes
physiological function
ubiquitin C-terminal hydrolase UCH-L3 is upregulated in normal or non-metastatic prostate cancer cells and is downregulated in metastatic prostate cancer cell lines. Knockdown of UCH-L3 in normal prostate cell line RWPE1 promotes epithelial-to-mesenchymal transition, an important process for cancer cell invasion and metastasis. The induction of epithelial-to-mesenchymal transition by UCH-L3 knockdown results in an increase of cell migration and invasion. Overexpression of UCH-L3 in highly metastatic prostate cancer cell line PC3 reverses epithelial-to-mesenchymal transition but an active site mutant of UCH-L3 does not
physiological function
UCH-L1 physically interacts with CDK1, CDK4, and CDK5, enhancing their kinase activity
physiological function
-
UCHL5 is required for high glucose-induced reduction of TGFbetaR1 protein ubiquitination, p21WAF1 protein expression, cell hypertrophy and fibronectin protein expression
physiological function
major deubiquitinating enzyme of the nervous system and associated with the development of neurodegenerative diseases
physiological function
the enzyme is not essential for neuronal development but it is absolutely required for the maintenance of axonal integrity
physiological function
the enzyme is required for regulated protein degradation in the kidney by controlling proteasome abundance
physiological function
the enzyme plays a key role in angiogenesis by regulating hydrogen peroxide generated by NADPH oxidase 4
physiological function
UCH-L1 is required for the maintenance of axonal integrity
physiological function
UCH-L1 may play pathogenic roles in many neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease
physiological function
UCHL1 may play a role in myogenesis by promoting myoblast proliferation and inhibiting differentiation
physiological function
the enzyme is essential for viral replication
physiological function
-
UCH-L1 mediates maintenance of the temporal integrity and persistence of cyclic AMP response element binding protein, CREB, phosphorylation in the brain
-
physiological function
-
UCHL1 is a component of the ubiquitin system, and the UCH-L1-dependent apoptosis is important for spermatogenesis. UCH-L1 plays an important role, possibly in association with Jab1 and p27Kip1, in selective elimination of abnormal oocytes during mouse prepubertal development
-
physiological function
-
UCHL5 is involved in the ubiquitin-proteasome pathway
-
additional information
-
activity of UCHL1 stimulates ligase activity of this enzyme in bovine oocytes, resulting in increased protein stabilization or modification through K63-linked polyubiquitination
additional information
-
autoantigenicity of UCH-L1: UCH-L1 is an antigen for autoantibodies in CNS-Lupus, systemic lupus erythematosus manifested in central nervous system, an autoimmune disease, overview
additional information
-
ectopic expression of UCH-L3 promotes the phosphorylation of insulin/IGF-I receptor and adipocyte differentiation in fibroblasts, overview
additional information
-
membrane-associated farnesylated UCH-L1 promotes alpha-synuclein neurotoxicity, mechanism, overview
additional information
-
membrane-associated farnesylated UCH-L1 promotes alpha-synuclein neurotoxicity, mechanism, overview
additional information
UCHL1 is a Parkinson disease-associated, putative cysteine protease
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C132A
-
site-directed mutagenesis, the mutant behaves similar to the wild-type enzyme
C132S
-
no effect on protein insolubility or interactions
C152A
-
site-directed mutagenesis, removal of the C152 thiol group by mutation renders the protein refractory to attack by 15-deoxy-DELTA12,14-prostaglandin J2
C152S
-
binds to monoubiquitin in both 4-hydroxy-2-nonenal-treated cells and untreated cells
C201A
-
site-directed mutagenesis, the mutant behaves similar to the wild-type enzyme
C209S
-
catalytically inactive, does not suppress NF-kappaB nuclear translocation and transcriptional activity by targeting the TNFR signaling pathway at the level of the IkappaB kinase complex or upstream from it. Does not suppress polyubiquitinated RIP1 and does not enhance the levels of monubiquinated or unmodified RIP1 as compared to the wild-type
C220A
-
site-directed mutagenesis, the mutant behaves similar to the wild-type enzyme
C335S
-
site-directed mutagenesis of active site Cys335, unaltered substrate binding
C37A
site-directed mutagenesis
C47A
-
site-directed mutagenesis, the mutant behaves similar to the wild-type enzyme
C786A
site-directed mutagenesis, no activity
C90A
-
site-directed mutagenesis, the mutant behaves similar to the wild-type enzyme
C90S/K157R
-
reduces monoubiquitination
C91A
catalytically inactive mutant, can still associate with the HCF-1 beta-propeller but cannot remove ubiquitin chains
C95A
enhances the interaction of ubiquitin dimers with UCH-L3
D176A
mutant shows an increased interaction with CDK4 compared to wild-type
D176N
-
site-directed mutagenesis, isozyme L1, 97.5% reduced activity compared to wild-type
D30A
-
site-directed mutagenesis, the mutant enzyme shows highly reduced hydrolase and ubiquitin binding activity
D33A
ubiquitin affinity deficient mutant, diminishes the interaction of ubiquitin dimers with UCH-L3
D348A
-
site-directed mutagenesis, inactive mutant, leads to accumulation of ubiquitin on endosomes and the concomitant stabilization of an ubiquinated form of the signal transducing adeptor molecule, STAM
DELTA148-190
deletion mutant containing amino acids 148-190 interacts with CDK4
DELTA148-223
deletion mutant containing amino acids 148-223 interacts with CDK4
DELTA160-190
deletion mutant containing amino acids 160-190 interacts with CDK4
DELTA160-223
deletion mutant containing amino acids 160-223 interacts with CDK4
DELTA188-223
deletion mutant containing amino acids 188-223 does not interact with CDK4
E174A
mutant shows an increased interaction with CDK4 compared to wild-type
E7A
point mutation in UCH-L1 is identified as the cause of early onset neurodegeneration in three siblings who appear normal at birth, but became blind at 5 years old and suffer progressive neurological dysfunction and cerebellar ataxia, and are unable to stand by the age of 30
F214A
the F214A mutant binds with approximately 60fold less affinity to ubiquitin compared to the wild-type UCH-L1, it shows highly reduced activity compared tot he wild-type enzyme
H165A
mutant shows an increased interaction with CDK4 compared to wild-type
H185A
-
displays increased interactions with tubulin
Q37R
-
site-directed mutagenesis, isozyme L1, unaltered activity
Q82A
kcat and Km can not be determined individually because, even at concentrations of ubiquitin 7-amido-4-methylcoumarin as high as 12 microM, the Michaelis-Menten plot is still rising linearly with substrate concentration, not reaching the plateau that is diagnostic of saturation
Q84A
Km (ubiquitin 7-amido-4-methylcoumarin) increased compared to wild-type, kcat (ubiquitin 7-amido-4-methylcoumarin) decreased
Q89A
Km (ubiquitin 7-amido-4-methylcoumarin) increased compared to wild-type, kcat (ubiquitin 7-amido-4-methylcoumarin) decreased
S18Y/I93M
-
increased insolubility
C61S
loss of deubiquitinating enzyme activity, does not decrease viral ribonucleotide reductase activity
C14A
mutant of ataxin-3 carrying six consecutive glutamines, does not undergo proteolytic fragmentation on incubation at room temperature
C14A/H119L
mutant of ataxin-3 carrying six consecutive glutamines, does not undergo proteolytic fragmentation on incubation at room temperature
C95S
retains the affinity to interact with ubiquitin dimers
D30K
site-directed mutagenesis, isozyme L1, inactive
D33A
loses the affinity to interact with ubiquitin dimers. D33A mutant expressing cells do not show any signs of free ubiquitin dimers accumulation
H119L
mutant of ataxin-3 carrying six consecutive glutamines, does not undergo proteolytic fragmentation on incubation at room temperature
S18Y
mutant of the Uch-L1 protein fused to the transduction domain of HIV-transactivator protein, has similar hydrolase activity than the unmutated fusion protein
C545A
catalytically inactive USP19 mutant, destabilizes ubiquitin ligase KPC1
C571S
-
is unable to maintain normal ubiquitin levels. In doa4delta cells expressing C571S, CPS is missorted to the limiting membrane of the vacuole
doa4delta
-
defect in endosomal localization
W782R
-
is solely cytoplasmic, defect in endosomal localization, Bro1-Doa4 interaction is disrupted
C220S
sie-directed mutagenesis, structure analysis in comparison to the wild-type enzyme
C220S
-
no effect on protein insolubility or interactions
C220S
-
the mutant has in vitro ubiquitin hydrolase activity comparable to the wild-type protein
C88A
is inactive
C88A
mutant structure determination and comparison to the wild-type enzyme
C90S
-
site-directed mutagenesis, isozyme L1, inactive
C90S
site-directed mutagenesis, isozyme L1, inactive
C90S
exchange of the active site cysteine
C90S
-
site-directed mutagenesis, the mutant enzyme lacks C-terminal hydrolase activity but retains ubiquitin binding activity, the mutant shows similar physiological effects in recombinant transfected cells as the wild-type enzyme, overview
C90S
-
site-directed mutagenesis, the mutant enzyme shows no hydrolase and ubiquitin binding activity
C90S
-
increases cellular monoubiquitin levels, 30% is monoubiquitinated, whereas only 5-10% of wild-type is monoubiquitinated
C90S
-
lacks hydrolase activity but maintains binding affinity for ubiquitin, does not exhibit notably increased insolubility upon 4-hydroxy-2-nonenal-treatment compared with UCH-L1 wild-type, has no effect on the interaction of UCH-L1 and tubulin
C90S
a catalytically inactive mutant of UCHL1
C90S
-
a UCH L1 mutant, that shows no binding to beta-catenin
C90S
mutant shows same interaction pattern as wild-type. Mutant shows no hydrolase activity
C95S
active site mutant of UCH-L1
C95S
active site mutant of UCH-L3, enhances the interaction of ubiquitin dimers with UCH-L3
C95S
active-site mutant. In highly metastatic prostate PC-3 cells, presence of UCH-L3 inhibits the cell migration and invasion but mutant C95S has no effects
D30K
-
deficient in ubiquitin binding, is unable to increase cellular monoubiquitin levels
D30K
-
lacks hydrolase activity and binding affinity for ubiquitin, has no effect on the interaction of UCH-L1 and tubulin
H161D
-
site-directed mutagenesis, isozyme L1, very low activity
H161D
-
30% is monoubiquitinated, whereas only 5-10% of wild-type is monoubiquitinated
H161D
-
a UCH L1 mutant, that shows no binding to beta-catenin
H161K
-
catalytically inactive
H161K
-
site-directed mutagenesis, isozyme L1, nearly inactive
H161N
-
catalytically inactive
H161N
-
site-directed mutagenesis, isozyme L1, nearly inactive
H161Q
-
catalytically inactive
H161Q
-
site-directed mutagenesis, isozyme L1, nearly inactive
H161Y
-
catalytically inactive
H161Y
-
site-directed mutagenesis, isozyme L1, nearly inactive
H97N
-
85% activity compared to wild-type
H97N
-
site-directed mutagenesis, isozyme L1, slightly reduced activity
H97Q
-
85% activity compared to wild-type
H97Q
-
site-directed mutagenesis, isozyme L1, slightly reduced activity
I93M
site-directed mutagenesis, isozyme L1, mutant shows increased risk for Parkinson's disease, 45.6% enzyme activity compared to wild-type
I93M
-
the mutation is linked to familial Parkinson's disease, the mutant dimer conformation is different from the wild-type enzyme deforming the globular form
I93M
-
wild-type enzyme, mutant I93M (linked to familial Parkinson's disease) and S18Y (linked to reduced risk of Parkinson's disease) are all self-assembled dimers. The configuration of these dimers are quite different. The wild-type is a rotating ellipsoidal
I93M
-
approximately doubles the monoubiquitination level of UCH-L1
I93M
-
missense mutation in the UCH-L1 gene in a German family with a familial case of Parkinson´s disease, decreases hydrolytic activity
I93M
-
mutation in UCH-L1 associated with familial Parkinsons disease, shows increased insolubility and elevated interactions with multiple proteins, promotes tubulin polymerization
I93M
-
naturally occuring mutation involved in Parkinson's disease
I93M
naturally occuring mutation of Uch-L1 involved in the Parkinson's disease
I93M
the mutant is a Parkinson disease-associated variant of UCH-L1, structure determination and comparison
I93M
-
the UCH-L1 mutant is associated with Parkinson's disease. The mutant enzyme protein is well-folded, structurally similar to the wild-type protein, and aggregates upon conjugation by cyclopentenone prostaglandins
I93M
mutant shows a stronger interaction with CDK1, CDK4 and CDK5 compared to wild-type. Hydrolase and ligase activity are reduced in mutant compared to wild-type
I93M
transgenic mice expressing the human I93M gene are born normally and are fertile. They do display aberrant dopaminergic neuron morphology in the substantia nigra at 12 weeks, consistent with degeneration and a loss of dopaminergic neurons at 20 weeks. The I93M mutation decreases UCHL1 solubility, corresponding with an apparent loss of alpha-helical structure seen via circular dichroism, and a reduction in hydrolytic activity by approximately 50%
R63A
-
displays increased interactions with tubulin, causes a decrease in tubulin polymerization
R63A
mutant shows an increased interaction with CDK4 compared to wild-type
S18Y
site-directed mutagenesis, isozyme L1, mutant shows decreased risk for Parkinson's disease, 112.6% enzyme activity compared to wild-type
S18Y
sie-directed mutagenesis, structure analysis in comparison to the wild-type enzyme
S18Y
-
the mutation is linked to reduced risk of Parkinson's disease, the mutant dimer conformation is different from the wild-type enzyme promoting the globularitiy
S18Y
variant of the ubiquitin carboxy-terminal hydrolase L1 gene is associated with Parkinson's disease
S18Y
-
wild-type enzyme, mutant I93M (linked to familial Parkinson's disease) and S18Y (linked to reduced risk of Parkinson's disease) are all self-assembled dimers. The configuration of these dimers are quite different. The wild-type is a rotating ellipsoidal
S18Y
-
does not affect cellular levels of monoubiquitinated UCH-L1
S18Y
monomeric in solution
S18Y
-
reduces risk of Parkinson´s disease. The protective role reflects a restricted mechanism only applied in sporadic Parkinson´s disease patients. The mutant is less likely to form dimers. Mutation also present in patients with earlier/later onset of Huntington´s disease
S18Y
-
UCH-L1 mutant with protective effect, is significantly inversely associated with sporadic Parkinson's disease in Sweden and with a low age of onset (less-than-or-equal 50 years)
S18Y
-
a naturally occuring polymorph, replacing the weak CKAA farnesylation motif with the optimal CVIM motif (S18Y/CVIM UCH-L1) leads to significantly increased accumulation of alpha-synuclein relative to S18Y
S18Y
a naturally occuring UCHL1 polymorphism, genotyping and allele frequencies in healthy persons and Alzheimer's disease patients of Swedish population, overview. The UCHL1 S18Y polymorphism does not show a protective effect against Alzheimer's disease
S18Y
-
naturally occuring mutation involved in Parkinson's disease
S18Y
naturally occuring mutation of Uch-L1 involved in the Huntington's disease
S18Y
the mutant is a Parkinson disease-associated variant of UCH-L1, structure determination and comparison
S18Y
mutation in UCH-L1 exerts a neuroprotective effect against Parkinson's disease. The S18Y mutant is initially reported as a polymorphism, present in approximately 46-61% of those studied in Asian populations, and 16-24% in European Caucasian populations who show a reduced risk of Parkinson's disease
C90S
site-directed mutagenesis, isozyme L1, inactive
C90S
exchange of the active site cysteine
C90S
-
inhibits the protective action of endogenous UCH-L1. C90S-fusion protein does not rescue the deficit in long term potentiation induced by Abeta, acts as a dominant negative mutant, causes a deficit in long term potentiation in the absence of oligomeric Abeta
C90S
mutant of the Uch-L1 protein fused to the transduction domain of HIV-transactivator protein, has little activity
additional information
-
gene cyk-3 null mutants are lethal, mutants fail to polarize the actin cytoskeleton, to segregate germline determinants, to assemble an intact cleavage furrow, and are intrinsically defective in osmotic regulation and cytokinesis, the latter defect can be partially rescued by providing osmotic support
additional information
-
enzyme downregulation in HeLa cells by siRNA, enzyme inhibition influences the degradation of the EGF receptor
additional information
-
silencing of UCH-L1 by expression of siRNA in H1299 cells
additional information
-
fusion protein UbVV/L8A-UCH-L1 contains an L8A mutation in the ubiquitin moiety. Efficiently binds ubiquitin, increases cellular monoubiquitin levels
additional information
-
model simulations indicate that mutation in UCH-L1 causes more rapid accumulation and aggregation of alpha-synuclein than occurs in the sporadic forms of Parkinson´s disease
additional information
-
a catalytic mutant has no effect on proliferation of a UCH-L1 negative EBV transformed lymphoblastoid cell line and on inhibiting cell adhesion
additional information
a catalytic mutant has no effect on proliferation of a UCH-L1 negative EBV transformed lymphoblastoid cell line and on inhibiting cell adhesion
additional information
wild type Bap1 and the NHNY/AAAA mutant display robust activity. Mutation of the NHNY sequence abolishes the association with HCF-1 but does not alter the intrinsic enzymatic activity of the ubiquitin C-terminal hydrolase domain
additional information
-
gene rs5030732, genotyping and UCHL1 polymorphisms, expression analysis, overview
additional information
-
knockdown of UCH-L1 by RNAi inhibits the proliferation of Burkitt's lymphoma cells in suspension and semisolid agar and activates strong LFA-1-dependent homotypic adhesion. Recombinant expression of a catalytically active UCH-L1 promotes the proliferation of a UCH-L1-negative EBV transformed lymphoblastoid cell line, LCL, and inhibited cell adhesion, whereas a catalytic mutant has no effect
additional information
knockdown of UCH-L1 by RNAi inhibits the proliferation of Burkitt's lymphoma cells in suspension and semisolid agar and activates strong LFA-1-dependent homotypic adhesion. Recombinant expression of a catalytically active UCH-L1 promotes the proliferation of a UCH-L1-negative EBV transformed lymphoblastoid cell line, LCL, and inhibited cell adhesion, whereas a catalytic mutant has no effect
additional information
-
UCH L1 silencing with siRNAs leads to accumulation of beta-catenin
additional information
C-terminal deletion of the final four Rrsidues of isoform UCH-L1 (CKAA) leads to increased membrane association and decreased solubility. Deletion disrupts the protein secondary structure, leads to abrogation of substrate binding, increased cell death, and an abnormal intracellular distribution
additional information
-
gad mouse null mutants of isozyme L1 show reduced monoubiquitin level in neurons, overexpression of the isozyme L1 leads to an increased monoubiquitin level
additional information
gad mouse null mutants of isozyme L1 show reduced monoubiquitin level in neurons, overexpression of the isozyme L1 leads to an increased monoubiquitin level
additional information
-
gad, i.e. gracile axonal dystrophy, mice testis lack isozyme UCH-L1
additional information
gad, i.e. gracile axonal dystrophy, mice testis lack isozyme UCH-L1
additional information
-
gad, i.e. gracile axonal dystrophy, mice testis lack isozyme UCH-L1 and are resistant to cryptorchid stress-related injury, the show reduced ubiquitin levels, uchl3 knockout mice show profound testicular atrophy and apoptotic germ cell loss after cryptorchid injury, but unaltered ubiquitin levels compared to wild-type mice, testicular phenotype of mutant mice, overview
additional information
gad, i.e. gracile axonal dystrophy, mice testis lack isozyme UCH-L1 and are resistant to cryptorchid stress-related injury, the show reduced ubiquitin levels, uchl3 knockout mice show profound testicular atrophy and apoptotic germ cell loss after cryptorchid injury, but unaltered ubiquitin levels compared to wild-type mice, testicular phenotype of mutant mice, overview
additional information
-
UCH-L1-deficient gad mice show progressively decreasing spermatogonial stem cell proliferation
additional information
UCH-L1-deficient gad mice show progressively decreasing spermatogonial stem cell proliferation
additional information
UCH-L1-deficient gad mice show progressively decreasing spermatogonial stem cell proliferation
additional information
-
in gracile axonal dystrophy mice with a spontaneous deletion in the Uch-l1 gene, memory in passive avoidance learning, exploratory behaviour and hippocampal CA1 long-term potentiation are reduced, whereas cyclic AMP response element binding protein phosphorylation is altered
additional information
-
mutant of the Uch-L1 protein fused to the transduction domain of HIV-transactivator protein with a 57 amino acid deletion (130-186) including the H161 site, is inactive
additional information
mutant of the Uch-L1 protein fused to the transduction domain of HIV-transactivator protein with a 57 amino acid deletion (130-186) including the H161 site, is inactive
additional information
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UCH-L1-deficient ova of gad female mice have a significantly increased rate of polyspermy in in vitro fertilization assays, although the rate of fertilization does not differ significantly from wild-type mice. Litter size of gad female mice is significantly reduced compared with wild-type mice
additional information
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Uchl3 deletion mutant displays retinal degeneration, muscular degeneration, and mild growth retardation. No significant morphological abnormalities during retinal development, prominent retinal degeneration becomes manifested after 3 weeks of age associated with photoreceptor cell apoptosis. Decreased area of mitochondrial cristae and vacuolar changes in the degenerated inner segment. Loss of UCH-L3 leads to mitochondrial oxidative stress-related photoreceptor cell apoptosis in a caspase-independent manner
additional information
mice with a genetic deficiency of CYLD have aberrant osteoclast differentiation and develop severe osteoporosis. Cultured osteoclast precursors derived from CYLD-deficient mice are hyperresponsive to RANKL-induced differentiation and produce more and larger osteoclasts than do controls upon stimulation
additional information
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construction of UCH-L1 knockout mice by targeted deletion of the UCH-L1 gene, in the absence of UCH-L1, synaptic transmission at the neuromuscular junctions is markedly impaired and it leads to ultrastructural defects of presynaptic nerve terminals at the neuromuscular junctions. UCH-L1 null mutation leads to progressive paralysis and premature death in mice, external phenotype and survival rate, overview
additional information
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deficiency of UCH-L1 of gad mice, i.e. UCH-L1-deficient mutant gracile axonal dystrophy mice, leads to vulnerability to lipid peroxidation both in vivo and in vitro. When neurons from dorsal root ganglions are cultured in the vitamin E-free medium, cell death is increased in the neurons of gad mice. Oxidative stress, especially lipid peroxidation, augments the neuronal cell death of gad mice
additional information
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embryonic fibroblasts from Uchl3-/- mice show an accumulation of polyubiquitinated proteins, the polyubiquitinated protein accumulation in Uchl3-/- embryonic fibroblasts is attenuated by the exogenous expression of wild-type, but not hydrolase activity deficient UCH-L3, overview
additional information
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enzyme downregulation by RNAi. UCH L1 suppression inhibits cell proliferation and migration and induces G0/G1 arrest and apoptosis
additional information
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gad, i.e. gracile axonal dystrophy, mice are analogous to a null mutants of UCH-L1, they display the dying-back-type of axonal degeneration in sensory neurons. The level of mono-ubiquitin is decreased in neurons, especially in axons of the sciatic nerve, in gad mice
additional information
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in UCH-L3 knockout mice, the levels of both Nedd8 and the apoptotic protein p53 and Bax are elevated upon cryptorchid injury, the accumulation of Nedd8-conjugated proteins in UCH-L3 knockout mice contributed to profound germ cell loss via apoptosis
additional information
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isolated loss of UCHL1/PGP 9.5 function, seen in the gracile axonal dystrophy, GAD, mouse due to a deletion in its gene results in a failure of axonal transport and a dying-back axonopathy beginning distally in long axons, the characteristic lesion in the GAD mouse is axonal dystrophy, gad mouse neuronal function phenotype, detailed overview
additional information
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melanopsin-Ir is significantly reduced in the retina of gracile axonal dystrophy, i.e. gad, mice with a spontaneous deletion in the Uch-l1 gene, resulting in impairment of circadian light perception in gad mice, overview. In constant darkness, gad mice show circadian rhythms in locomotor activity, indicating the integrity of the endogenous circadian rhythm generator. In addition, gad mice show increased locomotor activity in the light period when kept in a standard photoperiod and entrainment to phase shifts is significantly slower than in wild-type mice
additional information
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UCHL1-deficient gracile axonal dystrophy, i.e. gad, mice are spontaneous mutants with an in-frame deletion in exons 7 and 8 of Uch-l1. Deletion of the gene encoding UCH-L1 leads to a reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice, overview
additional information
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Uchl3-deficient mice show reduced content of white adipose tissue and reduced adipogenesis due to attenuated insulin responses, ectopic expression of wild-type UCH-L3 restores the phosphorylation of insulin/IGF-I receptor and adipocyte differentiation in UCH-L3-/- mouse embyronic fibroblasts, overview. Hydrolase-deficient UCH-L3 does not enhance insulin signalling and expression of gluta4, fabp4, and adiponectin, resulting in impaired formation of large lipid droplets
additional information
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in gracile axonal dystrophy mice with a spontaneous deletion in the Uch-l1 gene, memory in passive avoidance learning, exploratory behaviour and hippocampal CA1 long-term potentiation are reduced, whereas cyclic AMP response element binding protein phosphorylation is altered
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additional information
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UCHL1-deficient gracile axonal dystrophy, i.e. gad, mice are spontaneous mutants with an in-frame deletion in exons 7 and 8 of Uch-l1. Deletion of the gene encoding UCH-L1 leads to a reduction in memory in passive avoidance learning, exploratory behaviour and synaptic plasticity in mice, overview
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additional information
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deficiency of UCH-L1 of gad mice, i.e. UCH-L1-deficient mutant gracile axonal dystrophy mice, leads to vulnerability to lipid peroxidation both in vivo and in vitro. When neurons from dorsal root ganglions are cultured in the vitamin E-free medium, cell death is increased in the neurons of gad mice. Oxidative stress, especially lipid peroxidation, augments the neuronal cell death of gad mice
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additional information
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additional information
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enzyme deficient strain accumulates membrane-bound ubiquitin-conjugated Fur4p
additional information
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multivesicular body sorting of Gap1 is defective in a doa4delta mutant, which is not suppressed by restoring the ubiquitin pool. In the doa4delta ypt6delta strain, the pool of monomeric ubiquitin is as reduced as in the single doa4delta mutant
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molecular biology
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Pichia pastoris is a robust system to express the secreted form of Drosophila melanogaster UCH
synthesis
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used as molecular scissors for releasing a peptide or protein product
analysis
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the proportion of inclusion-bearing cells showing high levels of ubiquitin C-terminal hydrolase may provide a marker of the activity of a degenerative process
analysis
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UCH-L1 is a neuronal marker
degradation
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a natural dodecapeptide amide from UCH-L3 with the sequence DPDELRFNAIAL is capable of binding to monoubiquitin and may enable the design of peptides with different affinities towards K48- and K63-linked polyubiquitin
degradation
protein L-isoaspartate O-methyltransferase initiates the repair of isoaspartyl residues in aged or stress-damaged proteins in vivo, e.g. UCHL1 is a substrate for the L-isoaspartate methyltransferase in vivo
diagnostics
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ubiquitin C-terminal hydrolase is a biomarker in humans for severe traumatic brain injury
diagnostics
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UCH-L1 is a biomarker for ischemic and traumatic brain injury in rats
diagnostics
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UCH-L1 is a biomarker for lymph node metastasis in colorectal cancer
diagnostics
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UCHL1 is a potential cerebrospinal fluid biomarker of neuronal loss in aneurysmal subarachnoid hemorrhage and presumably other CNS damage and disease states, overview
drug development
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three-step docking (DOCK, rough GOLD, and fine GOLD) and in vitro enzyme assay methods to identify UCH-L3 inhibitors. UCH-L3 inhibitors may be useful for future apoptosis-inducing anti-cancer drug development
drug development
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UCH54, homologous to human UCH37, may represent a target for pharmacological intervention
drug development
the enzyme may contribute to the pathogenesis of idiopathic pulmonary fibrosis and may be a potential therapeutic target
medicine
ubiquitin hydrolase Uch-L1 could be an attractive target for the development of new therapeutic approaches to Alzheimer's disease
medicine
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activation of UCH-L1 may be a useful therapeutic approach for treating Alzheimers disease. Administration of a UCH-L1 fused to the transduction domain of the HIV-transactivator protein to supplement endogenous UCH-L1 has a protective effect on memory loss in a mouse model of Alzheimers disease. It restores long term potentiation and contextual memory to normal levels, whereas levels of the regulatory subunit of protein kinase A decrease, which, in turn, leads to increased levels of phosopho-cAMP response element binding protein
medicine
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class of 3-amino-2-keto-7H-thieno[2,3-b]pyridin-6-one derivatives as UCH-L1 inhibitors provide useful tools for investigating the role of UCH-L1 in normal cellular physiology, as well as in pathological conditions, such as Parkinsons disease and some forms of cancer
medicine
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expression of UCH-L1 is increased during long-term facilitation, which is related to synaptic plasticity and learning
medicine
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interactions of mutant or carbonyl-modified UCH-L1 with other proteins constitute one of the causes of not only familial Parkinsons disease, but also sporadic Parkinsons disease. Carbonyl-modified and mutant UCH-L1 share common properties, e.g. adopt a similar aberrant structure, promote tubulin polymerization, show decreased ubiquitin binding, and both increased insolubility and interactions with proteins over 30 kDa compared with the wild-type
medicine
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overexpression in chronic smokers may represent an early event in the complex transformation from normal epithelium to overt malignancy
medicine
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overexpression of UCHL1 significantly attenuates tumor necrosis factor-alphainduced nuclear factor-kappa B activity in vascular cells and increases inhibitor of kappa B-alpha, possibly through the attenuation of kappa B-alpha ubiquitination, leading to decreased neointima in the balloon-injured artery
medicine
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Parkinson disease-associated UCH-L1 is regulated by reversible monoubiquitination involving auto-deubiquitination
medicine
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possible involvement of UCH-L1 and UCH-L3 in the pathogenesis and progression of breast cancer. High UCH-L1 mRNA level is significantly associated with negative estrogen receptor status and negative progesterone receptor status. Patients with both UCH-L1 and UCH-L3 mRNA high tumors show a significantly poorer prognosis than those in the UCH-L1 or UCH-L3 mRNA low group
medicine
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sperm acrosomal UCHs are involved in sperm-zona pellucida interactions and antipolyspermy defense. Modulation of spermal UCH activity may facilitate the management of polyspermy during in vitro fertilization and provide insights into male fertility. Recombinant UCHs reduce polyspermy and proportionally increase the rate of monospermic fertilization during in vitro fertilization. Oocyte-secreted UCHs are not necessary for antipolyspermy defense during in vitro fertilization
medicine
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targeting the UCH37-Smad7 complex may provide a new approach for treating human diseases in which there is overt up-regulation in TGF-beta signalling activity. Competing effects of ubiquitin ligases and DUBs in complex with Smad7 can serve to fine-tune responses to TGF-betas under various physiological and pathological conditions
medicine
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transient ischemia induces selective delayed motor neuronal death and affects the profile of expression of ubiquitin, parkin, and UCH-L1. Vulnerability of motor neuron of the spinal cord may be partially attributed to the different response in ubiquitin-mediated stress response after transient ischemia
medicine
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UCH-L1 deficiency and impairment of the ubiquitin-dependent protein degradation pathway contributes to increased cell death observed in many lysosomal storage disorders
medicine
UCH-L1 deficiency and impairment of the ubiquitin-dependent protein degradation pathway contributes to increased cell death observed in many lysosomal storage disorders
medicine
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UCH-L1 has a putative but still undefined role in the ubiquitin-dependent protein degradation pathway. Postmortem analysis of human brains shows this pathway to be compromised in Alzheimers disease. A polymorphism in the UCH-L1 gene increases the risk of Alzheimers disease in females and also effects the risk of Parkinsons disease in Asian populations
medicine
UCH-L1 is a potent molecular biomarker for monitoring early stage of neurodegeneration occurring under oxidative stress in elderly people of advanced age
medicine
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UCH-L1 is an important component of the ubiquitin-proteasome system and is linked to Parkinson´s, Huntington´s, Alzheimer´s disease and other neurodegenerative disorders. UCH-L1 is an attractive target for the development of new therapeutic approaches to Alzheimer´s disease
medicine
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UCH-L1 is required for maintenance of memory in a passive avoidance test, exploratory behaviour in a novel environment, and a transcription-dependent component of theta-burst stimulation-induced long-term potentiation in area CA1 of the hippocampus
medicine
Uch-L1 is required for normal synaptic and cognitive function. Uch-L1 activity plays a role in normal contextual fear learning. Transduction of Uch-L1 protein fused to the transduction domain of HIV-transactivator protein restores normal enzymatic activity and synaptic function both in hippocampal slices treated with oligomeric Ab and in the APP/PS1 mouse model of Alzheimers disease. Intraperitoneal injections with the fusion protein improve the retention of contextual learning in APP/PS1 mice over time. Beneficial effect of the Uch-L1 fusion protein is associated with restoration of normal levels of the protein kinase A-regulatory subunit IIa, PKA activity, and cAMP response element binding protein phosphorylation
medicine
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UCH-L1 is selectively expressed on the plasma membrane of mouse ova, where it may regulate membrane penetration by spermatozoa. The unique expression patterns of UCH-L1 and UCH-L3 suggest that these proteins have distinct functions during oogenesis and embryogenesis. UCH-L1 functions in the polyspermy block during mammalian fertilization
medicine
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UCHL-1 expression is a contributory factor in the abnormal protein aggregation in dementia with Lewy bodies. Putative therapeutic target in the treatment of dementia with Lewy bodies
medicine
UCHL1 is aberrantly regulated in frontotemporal dementia and parkinsonism linked to chromosome 17
medicine
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Uchl3-deficient mice represent a model for adultonset retinal degeneration associated with mitochondrial impairment
medicine
mono-ubiquitin and ubiquitin dimers may regulate the enzymatic functions of UCH-L1 in vivo
medicine
UCH-L1 expression seems to be associated with the metastatic potential of human renal cell carcinoma cell SN12C clones
medicine
uchl1 genes as novel targets of alpha-tocopherol deficiency may offer molecular correlates of well documented descriptions of neuromuscular dysfunctions in alpha-tocopherol-deficient rodents
medicine
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membrane-associated farnesylated UCH-L1 is a therapeutic target for Parkinson's disease
medicine
expression of isoform UCHL1 is elevated in osteosarcoma compared with normal bone tissue. UCHL1 expression level is correlated with tumor maximum diameter, high rate of lung metastases and short survival time. Knockdown of UCHL1 in osteosarcoma cell MG-63 inhibits cell proliferation and significantly increases cell population in the G1 phase. Cyclins promoting G1/S phase transition are reduced after UCHL1 knockdown, including cell cycle regulator cyclin D1, cyclin E1 and CDK6. Inhibition of UCHL1 in MG-63 cells dramatically induces cell apoptosis. Downregulation of UCHL1 in MG-63 significantly inhibits cell invasion. There is a positive correlation between UCHL1 expression level and the Akt and ERK phosphorylation status
medicine
melanoma cells show a a widespread loss or reduced expression of ubiquitin C-terminal hydrolase UCHL1, which is directly correlated with promoter DNA hypermethylation. The subset of melanoma cells, which still express UCHL1, shows altered growth properties and tolerances against reactive oxygen species as compared to UCHL1-negative cells. UCHL1 may function as a new diagnostic biomarker or therapeutic target for the treatment of UCHL1-positive melanomas
medicine
ubiquitin C-terminal hydrolase UCH-L3 is upregulated in normal or non-metastatic prostate cancer cells and is downregulated in metastatic prostate cancer cell lines. Knockdown of UCH-L3 in normal prostate cell line RWPE1 promotes epithelial-to-mesenchymal transition, an important process for cancer cell invasion and metastasis. The induction of epithelial-to-mesenchymal transition by UCH-L3 knockdown results in an increase of cell migration and invasion. Overexpression of UCH-L3 in highly metastatic prostate cancer cell line PC3 reverses epithelial-to-mesenchymal transition but an active site mutant of UCH-L3 does not
medicine
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UCH-L1 is required for maintenance of memory in a passive avoidance test, exploratory behaviour in a novel environment, and a transcription-dependent component of theta-burst stimulation-induced long-term potentiation in area CA1 of the hippocampus
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pharmacology
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enzyme is a target for the development of antineoplastic agents
pharmacology
covalent docking plus MD refinement of a representative set of known SARS-CoV inhibitors into OTUB2, OTUB1, and the PLpro from SARS-CoV-2 to probe their inhibitor binding and rationalize a deubiquitinase selectivity. It is pointed out that the structural differences in cellular deubiquitinases suggest that these enzymes may be different enough to be selectively targeted
additional information
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the enzyme and the zebrafish can be utilized as an animal model for analysis of development of Parkinson's disease
additional information
the enzyme and the zebrafish can be utilized as an animal model for analysis of development of Parkinson's disease
additional information
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direct role of Doa4 in multivesicular body sorting pathway that is linked to its catalytic activity. Doa4 mediates a deubiquitination step required for sorting of CPS into the multivesicular body pathway
additional information
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dynamic regulation of apically located epithelial sodium channel by recycling, which is facilitated by UCH-L3
additional information
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essential role of UCH-L1 in oocyte maturation and in the completion of the first meiosis and its transition to anaphase
additional information
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UCH-L1 and UCH-L3 may have a role in growth transformation
additional information
Uch37 is responsible for isopeptidase activity
additional information
UCHL1 is a candidate aging-related protein
additional information
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UCHL1 is related to cellular senescence process
additional information
YUH effciently cleaves the ubiquitin-piscidin fusion protein, and since it can easily be prepared in the lab, it provides a cost-effective way of preparing the antimicrobial target peptide piscidin as compared to other systems
additional information
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YUH effciently cleaves the ubiquitin-piscidin fusion protein, and since it can easily be prepared in the lab, it provides a cost-effective way of preparing the antimicrobial target peptide piscidin as compared to other systems
additional information
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UCHL1 is related to cellular senescence process
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