3.4.22.59: caspase-6
This is an abbreviated version!
For detailed information about caspase-6, go to the full flat file.
Word Map on EC 3.4.22.59
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3.4.22.59
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caspases
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bcl-2
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alzheimer
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neurodegenerative
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pro-apoptotic
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huntington
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lamins
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apoptosis-related
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parp
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executioner
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caspase-dependent
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anti-apoptotic
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polyadp-ribose
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tunel
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caspase-mediated
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casps
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jurkat
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bid
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pan-caspase
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zvad-fmk
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apaf-1
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medicine
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procaspase-3
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fadd
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diagnostics
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fas-associated
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drug development
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molecular biology
- 3.4.22.59
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caspases
- bcl-2
- alzheimer
- neurodegenerative
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pro-apoptotic
- huntington
- lamins
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apoptosis-related
- parp
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executioner
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caspase-dependent
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anti-apoptotic
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polyadp-ribose
-
tunel
-
caspase-mediated
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casps
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jurkat
- bid
-
pan-caspase
- zvad-fmk
- apaf-1
- medicine
- procaspase-3
- fadd
- diagnostics
-
fas-associated
- drug development
- molecular biology
Reaction
strict requirement for Asp at position P1 and has a preferred cleavage sequence of Val-Glu-His-Asp-/- =
Synonyms
apoptotic protease Mch-2, C14.005, Cas6, Casp-6, Casp.6, Casp6, caspase 6, caspase-6, caspase-6A, caspase-6B, Csp-6, Csp6, HLcaspase-6, MCH2, Pfcasp-6, VEIDase
ECTree
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Natural Substrates Products
Natural Substrates Products on EC 3.4.22.59 - caspase-6
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REACTION DIAGRAM
Ac-Val-Glu-Ile-Asp-7-amido-4-trifluoromethylcoumarin + H2O
Ac-Val-Glu-Ile-Asp + 7-amino-4-trifluoromethylcoumarin
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beta-catenin + H2O
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processing of beta-catenin, production of a 70000 Da fragment
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cyclin B1 + H2O
truncated cyclin B1 + ?
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overriding the G2 DNA damage checkpoint permits precocious entry into mitosis that ultimately leads to mitotic catastrophe, caused by caffeine. Mitotic catastrophe is manifested by an unscheduled activation of CDK1, caspase activation and apoptotic cell death. Cyclin B1 is required for mitotic catastrophe, but is also cleaved into a 35 kDa protein by a caspase-dependent mechanism during the process, overview
expression of the truncated product enhanced cell death
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human telomerase + H2O
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caspase-6 cleaves human telomerase, hTERT, during apoptosis in cultured cells
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huntingtin + H2O
huntingtin peptide fragments
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a key step in the onset of Huntingtons disease is the caspase-6 mediated cleavage of the protein huntingtin into toxic fragments
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periplakin + H2O
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caspase 6 has a specific epidermal target which is periplakin
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poly(ADP-ribose)polymerase + H2O
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the enzyme may participate in poly(ADP-ribose)polymerase cleavage observed during apoptosis
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pro-caspase-6 + H2O
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caspase-8 activates caspase-3, and caspase-3 in turn activates caspase-6. Caspase 3 has a major role in nuclear apoptosis
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pro-caspase-8 + H2O
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caspase-6 is the major activator of caspase-8 in the cytochrome c-induced apoptosis pathway. Caspase-8 precursor is initially cleaved between the p18 and p10 domains resulting in fragments of 42000 Da and 10000 Da. The 42000 Da fragment is further cleaved resulting in fragments of 25000 Da and 18000 Da
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SATB1 + H2O
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cleavage disrupts PDZ domain-mediated dimerization, causing detachment from chromatin early in T-cell apoptosis
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Ufd2p + H2O
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cleavage of polyubiquitination factor Ufd2p at Asp123 within the putative regulatory N-terminal domain might have important functional consequences within the apoptotic cascade
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viral nucleocapsid protein of transmissible gastroenteritis coronovirus + H2O
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cleavage site VVPD359-/-. Destruction of viral protein by the host cell death machinery
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cleavage at the capase-6 consensus sequence at amino acid 586 in the nucleus, proteolysis of mutant huntingtin is crucial to the development of Huntington disease. Cell stress induced by staurosporine results in the nuclear translocation and activation of caspase-6 and increased cleavage of huntingtin, overview. Differential localization of different endogenous caspase-cleaved huntingtin fragments in perinuclear and nuclear regions, overview
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huntingtin + H2O
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cleavage at the capase-6 consensus sequence at amino acid 586 in the nucleus, proteolysis of mutant huntingtin is crucial to the development of Huntington disease. Cell stress induced by staurosporine results in the nuclear translocation and activation of caspase-6 and increased cleavage of huntingtin, overview. Differential localization of different endogenous caspase-cleaved huntingtin fragments in perinuclear and nuclear regions, overview
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caspase-6 + ?
the enzyme can self-process and self-activate
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pro-caspase-6 + H2O
caspase-6 + ?
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the enzyme can self-process and self-activate
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AP-2alpha is cleaved is at Asp19 of the sequence DRHD19 by caspase-6 before DNA framentation during TNF-alpha-induced apoptosis
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transcription factor AP-2alpha + H2O
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activates caspase-6 which in turn cleaves transcription factor AP2alpha
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the enzyme has a major role in nuclear apoptosis
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additional information
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bile acid-induced apoptosis, e.g. by glycochenodeoxycholic acid, in hepatocytes is caspase-6-dependent. Caspase-6 appears to play an important regulatory role in the promotion of bile acid-induced apoptosis as part of a feedback loop. Inhibition of caspase-9 reduces glycochenodeoxycholic acid-induced activation of caspase-6, whereas inhibition of caspase-6 reduces activation of caspase-8 placing caspase-6 between caspase-9 and caspase-8
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additional information
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caspase 6, an apoptosis-related cysteine peptidase, is upregulated in the skin of keloid prone patients. Caspase-6 plays a crucial role during apoptosis
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additional information
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caspase-6 activation occurs early in Alzheimer's disease and sometimes precedes the clinical manifestation of the disease in aged individuals. Early and neuritic activation of caspase-6 in Alzheimer disease can disrupt the cytoskeleton network of neurons, resulting in impaired neuronal structure and function in the absence of cell death. Proteomics analysis of caspase-6-mediated cleavage of human neuronal proteins, cleavage site determinations and cleavage specificity, overview
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additional information
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caspase-6 is a short pro-domain caspase that is activated early in Alzheimer disease, its activation does not induce apoptosis in HEK-293T cells, overview
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additional information
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possible involvement of caspase-6 and -7 but not caspase-3 in the regulation of hypoxia-induced apoptosis in tube-forming endothelial cells, caspase-6 is responsible for DNA ladder formation durirng hypoxia, overview
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additional information
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resveratrol-mediated activation of caspase-6 leads to apoptosis in HCT-116 colon cancer cells involving also p53, overview
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additional information
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ZBP-89, a Kruppel-type, zinc finger transcription factor, induces caspase-6 activation leading to inhibition of cell death in hepatoccellular carcinoma cells, inhibition of caspase-6 abolishes the effect of ZBP-89
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additional information
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development of an assay method for specifically detecting caspase-6 activity in an intact cell environment, evaluation of a 384-well whole-cell chemiluminescent ELISA assay that monitors the proteolytic degradation of endogenously expressed lamin A/C during the early stages of caspase-dependent apoptosis, overview
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additional information
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CLK3, alcohol dehydrogenase 4 and malate dehydrogenase 1B are not cleaved by caspase-6
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additional information
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the enzyme does not cleave receptor-interacting protein kinase-3
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additional information
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caspase 6 is an effector caspase in apoptosis pathways and regulates B cell activation and differentiation into plasma cells by modifying cell cycle entry, Casp6 is cleaved after B cell activation
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additional information
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caspase-6 is a key caspase known to play both initiator and effector roles in programmed cell death, excessive activation of the enzyme is an early marker of neuronal dysfunction and implicated in the pathogenesis of Huntington disease, Alzheimer's disease and other forms of cognitive impairment
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additional information
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development of an assay method for specifically detecting caspase-6 activity in an intact cell environment, evaluation of a 384-well whole-cell chemiluminescent ELISA assay that monitors the proteolytic degradation of endogenously expressed lamin A/C during the early stages of caspase-dependent apoptosis, overview
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additional information
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development of an assay method for specifically detecting caspase-6 activity in an intact cell environment, evaluation of a 384-well whole-cell chemiluminescent ELISA assay that monitors the proteolytic degradation of endogenously expressed lamin A/C during the early stages of caspase-dependent apoptosis, overview
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additional information
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caspase 6 is an effector caspase in apoptosis pathways and regulates B cell activation and differentiation into plasma cells by modifying cell cycle entry, Casp6 is cleaved after B cell activation
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additional information
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caspase-6 is a key caspase known to play both initiator and effector roles in programmed cell death, excessive activation of the enzyme is an early marker of neuronal dysfunction and implicated in the pathogenesis of Huntington disease, Alzheimer's disease and other forms of cognitive impairment
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additional information
?
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bile acid-induced apoptosis, e.g. by glycochenodeoxycholic acid, in hepatocytes is caspase-6-dependent. Caspase-6 appears to play an important regulatory role in the promotion of bile acid-induced apoptosis as part of a feedback loop. Inhibition of caspase-9 reduces glycochenodeoxycholic acid-induced activation of caspase-6, whereas inhibition of caspase-6 reduces activation of caspase-8 placing caspase-6 between caspase-9 and caspase-8
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