3.4.22.55: caspase-2
This is an abbreviated version!
For detailed information about caspase-2, go to the full flat file.
Word Map on EC 3.4.22.55
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3.4.22.55
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caspases
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bcl-2
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necrosis
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bid
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proapoptotic
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anti-apoptotic
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parp
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raidd
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apoptosis-inducing
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caspase-dependent
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z-vad-fmk
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p53-induced
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tunel
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jurkat
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polyadp-ribose
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casps
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mitochondria-mediated
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non-apoptotic
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pan-caspase
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apaf-1
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apoptosome
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caspase-mediated
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death-inducing
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cpp32
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fasl
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z-devd-fmk
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executioner
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xiap
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damage-induced
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etoposide-induced
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anti-fas
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prodomains
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p53-dependent
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trail-induced
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executor
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bh3-only
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ac-devd-cho
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apoptogenic
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trail-mediated
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procaspase
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caspase-10
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chk1
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beta-converting
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mitochondria-dependent
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medicine
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diagnostics
- 3.4.22.55
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caspases
- bcl-2
- necrosis
- bid
-
proapoptotic
-
anti-apoptotic
- parp
- raidd
-
apoptosis-inducing
-
caspase-dependent
- z-vad-fmk
-
p53-induced
-
tunel
-
jurkat
-
polyadp-ribose
-
casps
-
mitochondria-mediated
-
non-apoptotic
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pan-caspase
- apaf-1
- apoptosome
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caspase-mediated
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death-inducing
- cpp32
- fasl
- z-devd-fmk
-
executioner
- xiap
-
damage-induced
-
etoposide-induced
-
anti-fas
- prodomains
-
p53-dependent
-
trail-induced
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executor
-
bh3-only
- ac-devd-cho
-
apoptogenic
-
trail-mediated
-
procaspase
- caspase-10
- chk1
-
beta-converting
-
mitochondria-dependent
- medicine
- diagnostics
Reaction
strict requirement for an Asp residue at P1, with Asp316 being essential for proteolytic activity and has a preferred cleavage sequence of Val-Asp-Val-Ala-Asp-/- =
Synonyms
AjCASP, C14.006, CASP-2, Casp2, caspase 2, caspase-2, caspase-2L, caspase-2S, ICH-1, ICH-1 protease, ICH-1L/1S, NEDD-2
ECTree
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Source Tissue
Source Tissue on EC 3.4.22.55 - caspase-2
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treatment of melanoma cells with terfenadine induced DNA damage and caspases 2 activation. A selective inhibitor of caspase-2 (benzyloxycarbonyl-VDVAD-fluoromethylketone) protects melanoma cells from terfenadine-induced apoptosis
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histone deacetylase inhibition leads to decreased protein kinase casein kinase 2 activity, which is followed by caspase-2 activation and partial cleavage of caspase-8 that sensitizes the tumor cell to TRAIL-induced apoptosis
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PS-341 (bortezomib) induces a dose-dependent apoptosis in association with reactive oxygen species generation and cleavage of caspase-2 to its 33- and 14-kDa fragments. PS-341-induced caspase-2 activation is attenuated by a selective pharmacological inhibitor of cathepsin B (R-3032). Caspase-2 regulates mitochondrial permeability
immunostaining for caspase-2 increases as the luteal phase progresses
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thrombin initiates EMP generation from the human microvascular endothelial cell line HMEC-1. Caspase-2 plays a role in release of endothelial microparticles by controlling the proteolytic activation of ROCK-II
caspase-2 levels are significantly reduced in human lung adenocarcinoma with wild-type p53
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caspase 2 activation is required for release of cytochrome c and cell death
additional information
isoform casp-2S is undetectable in the SKOV3, H-1299 and HCT-116 p53-deficient cells
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expression of c-Myc and caspase-2 are crucial for cytochrome c release from mitochondria during cytotoxic stress. Caspase-2 is important for cytosolic Bax to integrate into the outer mitochondrial membrane
at estrus, activity is 7.6fold greater in the old corpus luteum compared to new corpus luteum
immunostaining for caspase-2 increases as the luteal phase progresses
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histone deacetylase inhibition leads to decreased protein kinase casein kinase 2 activity, which is followed by caspase-2 activation and partial cleavage of caspase-8 that sensitizes the tumor cell to TRAIL-induced apoptosis
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caspase-2 is required for apoptosis induced by cytoskeletal disruption. Caspase-2 mediates apoptosis via Piddosome, Bid and Bax activation, and cytochrome c release
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embryonic fibroblasts deficient for both Bax and Bak indicate the contribution of both Bax and Bak in mediating cell death induced by resveratrol and the existence of Bax/Bak-independent cell death possibly through caspase-8- or caspase-2-mediated mitochondria-independent downstream caspase processing
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caspase-2 activation occurs upstream of mitochondria in resveratrol-treated cells. The activated caspase-2 triggers mitochondrial apoptotic events by inducing conformational changes in Bax/Bak with subsequent release of cytochrome c, apoptosis-inducing factor, and endonuclease G. Caspase-2 contributes toward the mitochondrial translocation of Bid
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histone deacetylase inhibition leads to decreased protein kinase casein kinase 2 activity, which is followed by caspase-2 activation and partial cleavage of caspase-8 that sensitizes the tumor cell to TRAIL-induced apoptosis
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caspase-2L activationis induced by ionizing radiation (0.5 Gy) in the 1 day postpartum. Caspase-2-dependent activation of the mitochondrial apoptotic pathway is one of the mechanisms involved in the genotoxic stress-induced depletion of the primordial follicle pool
caspase-2 activity transiently increases more than two-fold within 24 h following induction of differentiation
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shift of caspase 2 from the cytoplasm in the sham-operated testis to the mitochondria in the testis after torsion