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3.4.21.53: Endopeptidase La

This is an abbreviated version!
For detailed information about Endopeptidase La, go to the full flat file.

Word Map on EC 3.4.21.53

Reaction

hydrolysis of proteins in presence of ATP =

Synonyms

AAA+ Lon protease, AAA+ protease, AAAP, AF0364, AfLon, archaeal Lon protease, ATP-dependent lon protease, ATP-dependent Lon proteinase, ATP-dependent PIM1 protease, ATP-dependent protease La, ATP-dependent protease lon, ATP-dependent protease LonA, ATP-dependent serine proteinase, ATP-independent Lon-like protease, bacterial protease lon, BPP1347, ClpXP, EcLon, Ec-Lon, Ec-Lon protease, EcLon, EcLon protease, ELon, Escherichia coli proteinase La, Escherichia coli serine proteinase La, Gene lon protease, Gene lon proteins, hLon, human ATP-dependent protease, human lon protease, HVO_0783, i-AAA Protease, la, La protease, lon, lon (la) protease, lon (Pim1p) protease, Lon AAA+ protease, lon ATP-dependent protease, lon protease, LON protease 1, Lon protein, Lon proteinase, lon-like protease, Lon-like-Ms, lon1, lon2, lon3, lon4, lonA, lonB, lonB protease, LonC, LonC protease, lonD, LONP1, lonR9, LONRF1, lonS, lonTK, lonV, mitochondrial ATP-dependent protease, mitochondrial ATP-dependent protease La, mitochondrial Lon protease, MLon, Ms-Lon, Msm 1754, Msm_1754, MtaLonA, MtaLonC, Nmag_2822, NmLon, non-canonical RNA viral Lon proteinase, peroxisomal Lon protease, PIM1, PIM1 protease, PIM1 proteinase, Pim1p, PLon, protease, Protease La, protease lon, Proteinase La, Proteinase, Escherichia coli serine, La, Proteinase, La, Proteins, gene lon, Proteins, specific or class, gene lon, ScLon, serine protease, Serine protease La, Ta1081, Thela2p4_005149, Thela2p4_006664, TK1264, TonLonB, TON_0529, yeast mitochondrial lon, yeast protease

ECTree

     3 Hydrolases
         3.4 Acting on peptide bonds (peptidases)
             3.4.21 Serine endopeptidases
                3.4.21.53 Endopeptidase La

Expression

Expression on EC 3.4.21.53 - Endopeptidase La

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
gene lon expression is under the control of CsrA, possibly at both the transcriptional and post-transcriptional levels. Transcription of lon is suppressed by CsrA
in muscle creatine kinase mouse heart model for Friedreich ataxia, a rare hereditary neurodegenerative disease characterized by progressive ataxia and cardiomyopathy, there is a clear progressive increase in protein levels of mitochondrial ATP-dependent proteases, Lon and ClpP, in the hearts of muscle creatine kinase mutants. Lon and ClpP upregulation, which is triggered at a mid-stage of the disease through separate pathways, is accompanied by an increase in proteolytic activity.
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Lon is upregulated after serum starvation
modest induction of mRNA after H2O2 treatment, with the highest inductions of 2.3fold at 4 h and 1.7fold at 7 h observed when the cells are treated with 0.100 mM H2O2 and 1.9fold at 4 h and 1.6fold at 7 h after 0.200 mM H2O2 treatment. Cells exposed to a 45°C heat shock exhibit an 80% induction of Lon protein after 1 h of shock, and 31% induction after 3 h recovery, gradually returning to basal levels at 6 and 24 h. Lon up-regulation by heat-shock is accompanied by a coinduction of mtHSP-70, which exhibits a 70% increase after 1 h of heat shock and declines to basal levels thereafter. Serum starvation stress for 1 h does not increase Lon levels. After recovery for 3 h in serum-supplemented medium, Lon protein levels exhibit a 4-fold increase. Lon protein levels after 6 and 24 h of serum starvation stress recovery remains relatively high, with protein inductions of about 3.8- and 3.1fold, respectively
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relative expression of Lon transcripts decreases by 2-fold after UV irradiation
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the cellular content of Lon mRNA varies in direct correlation with medium osmolarity, being the lowest under hyposalinity and the highest in 3.8 M NaCl (2-fold relative to 2.5 M respectively)
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