3.4.22.56: caspase-3
This is an abbreviated version!
For detailed information about caspase-3, go to the full flat file.
Word Map on EC 3.4.22.56
-
3.4.22.56
-
bcl-2
-
caspase-9
-
necrosis
-
tunel
-
parp
-
anti-apoptotic
-
neuroprotective
-
pro-apoptotic
-
tnf
-
endothelial
-
annexin
-
leukemia
-
apoptosis-related
-
mapks
-
fas
-
ischemia
-
dismutase
-
deoxynucleotidyl
-
erk
-
neurotoxicity
-
artery
-
cyclin
-
cerebral
-
dutp
-
malondialdehyde
-
reperfusion
-
infarct
-
nick
-
cardiac
-
sirna
-
apoptosis-inducing
-
myocardial
-
gsh
-
cardiomyocytes
-
sham
-
c-jun
-
cisplatin
-
survivin
-
transferase-mediated
-
iodide
-
hippocampal
-
adp-ribose
-
hoechst
-
antiproliferative
-
caspase-dependent
-
polyadp-ribose
-
bid
-
ischemia-reperfusion
-
propidium
-
ladder
-
analysis
-
drug development
-
molecular biology
-
medicine
-
diagnostics
- 3.4.22.56
- bcl-2
- caspase-9
- necrosis
-
tunel
- parp
-
anti-apoptotic
-
neuroprotective
-
pro-apoptotic
- tnf
- endothelial
-
annexin
- leukemia
-
apoptosis-related
- mapks
- fas
- ischemia
- dismutase
-
deoxynucleotidyl
- erk
-
neurotoxicity
- artery
- cyclin
- cerebral
- dutp
- malondialdehyde
-
reperfusion
- infarct
- nick
- cardiac
- sirna
-
apoptosis-inducing
- myocardial
- gsh
- cardiomyocytes
-
sham
- c-jun
- cisplatin
- survivin
-
transferase-mediated
- iodide
- hippocampal
- adp-ribose
-
hoechst
-
antiproliferative
-
caspase-dependent
-
polyadp-ribose
- bid
-
ischemia-reperfusion
- propidium
-
ladder
- analysis
- drug development
- molecular biology
- medicine
- diagnostics
Reaction
strict requirement for an Asp residue at positions P1 and P4. It has a preferred cleavage sequence of Asp-Xaa-Xaa-Asp-/- with a hydrophobic amino-acid residue at P2 and a hydrophilic amino-acid residue at P3, although Val or Ala are also accepted at this position =
Synonyms
apopain, C14.003, Cas-3, CASP-3, CASP3, caspase 3, caspase-3, CgCaspase-3, CPP-32, CPP32, CPP32/apopain, cystein aspartic-specific protease-3, cysteine aspartic acid-specific protease, cysteine protease CPP32, DEVDase, IRP, Lyccasp3, Mncaspase-3c, More, SBTc-3, SCA-1, SREBP cleavage activity 1, Yama protein, Yama/CPP32, ZCASP3
ECTree
3.4.22.56 caspase-3Advanced search results
results (
results (Substrates Products
Substrates Products on EC 3.4.22.56 - caspase-3
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SUBSTRATE 
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
Ac-Asp-Glu-Val-Asp-7-amido-4-methylcoumarin + H2O
Ac-Asp-Glu-Val-Asp + 7-amino-4-methylcoumarin
-
-
-
-
?
Ac-DEVD-4-methylcoumarin 7-amide + H2O
Ac-DEVD + 7-amino-4-methylcoumarin
-
an artificial caspase-3 substrate
-
-
?
Ac-DMQD-4-nitroanilide + H2O
Ac-DMQD + 4-nitroaniline
weak substrate
-
-
?
Ac-IETD-4-nitroanilide + H2O
Ac-IETD + 4-nitroaniline
an artificial caspase-8 substrate, low activity
-
-
?
Ac-LEHD-4-nitroanilide + H2O
Ac-LEHD + 4-nitroaniline
an artificial caspase-9 substrate, low activity
-
-
?
Ac-VDQQD-4-nitroanilide + H2O
Ac-VDQQD + 4-nitroaniline
weak substrate
-
-
?
acetyl-Asp-Glu-Val-Asp-4-nitroanilide + H2O
acetyl-Asp-Glu-Val-Asp + 4-nitroaniline
-
-
-
-
?
acetyl-Asp-Glu-Val-Asp-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-Asp-Glu-Val-Asp + 7-amino-4-trifluoromethylcoumarin
acetyl-DEVD-4-methylcoumarin-7-amide + H2O
acetyl-DEVD + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-DEVD-4-nitroanilide + H2O
acetyl-DEVD + 4-nitroaniline
-
-
-
-
?
acetyl-IETD-7-amido-4-methylcoumarin + H2O
acetyl-IETD + 7-amino-4-methylcoumarin
-
low activity towards the caspase-6 and caspase-8 substrate
-
-
?
acetyl-L-Asp-L-Glu-L-Val-L-Asp-4-nitroanilide + H2O
acetyl-L-Asp-L-Glu-L-Val-L-Asp + 4-nitroaniline
-
-
-
?
acetyl-L-Asp-L-Glu-L-Val-L-Asp-7-amido-4-methylcoumarin + H2O
acetyl-L-Asp-L-Glu-L-Val-L-Asp + 7-amino-4-methylcoumarin
-
-
-
?
acetyl-L-Asp-L-Met-L-Gln-L-Asp-4-nitroanilide + H2O
acetyl-L-Asp-L-Met-L-Gln-L-Asp + 4-nitroaniline
-
-
-
?
acetyl-L-Asp-L-Val-L-Ala-L-Asp-4-nitroanilide + H2O
acetyl-L-Asp-L-Val-L-Ala-L-Asp + 4-nitroaniline
-
-
-
?
acetyl-L-Leu-L-Asp-L-Val-L-Ala-L-Asp-4-nitroanilide + H2O
acetyl-L-Leu-L-Asp-L-Val-L-Ala-L-Asp + 4-nitroaniline
-
-
-
?
acetyl-L-Val-L-Asp-L-Val-L-Ala-L-Asp-4-nitroanilide + H2O
acetyl-L-Val-L-Asp-L-Val-L-Ala-L-Asp + 4-nitroaniline
-
-
-
?
acetyl-LEHD-4-methylcoumarin-7-amide + H2O
acetyl-LEHD + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-LEHD-7-amido-4-methylcoumarin + H2O
acetyl-LEHD + 7-amino-4-methylcoumarin
-
low activity towards the caspase-9 substrate
-
-
?
acetyl-VEID-4-methylcoumarin-7-amide + H2O
acetyl-VEID + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-YVAD-7-amido-4-methylcoumarin + H2O
acetyl-YVAD + 7-amino-4-methylcoumarin
-
low activity towards the caspase-1 substrate
-
-
?
anamorsin + H2O
?
-
specifically cleaved by caspase-3 at DSVD209 L generating 25- and 10-kDa fragments
-
-
?
benzoyl-L-Asp-L-Glu-L-Val-L-Asp-7-amido-4-methylcoumarin + H2O
benzoyl-L-Asp-L-Glu-L-Val-L-Asp + 7-amino-4-methylcoumarin
-
-
-
?
benzyloxycarbonyl-DEVD-7-amido-4-methylcoumarin + H2O
benzyloxycarbonyl-DEVD + 7-amino-4-methylcoumarin
-
-
-
-
?
beta-catenin + H2O
?
-
processing of beta-catenin, production of a 70000 Da fragment
-
-
?
caspase 9 + H2O
?
-
cleavage by caspase 3 does not result in activation of caspase 9, but enhances apoptosis by alleviating XIAP inhibition of the apical caspase
-
-
?
D4-GDI(Rho-GDI 2) + H2O
?
-
differential regulation of the homologous GDP dissociation inhibitors Rho-GDI 1 and D4-GDI during drug-induced apoptosis by proteolysis mediated by caspase-3
-
-
?
DEVD-7-amido-4-trifluoromethylcoumarin + H2O
DEVD + 7-amino-4-trifluoromethylcoumarin
-
-
-
-
?
DEVD-amido-4-trifluoromethylcoumarin + H2O
DEVD + amino-4-trifluoromethylcoumarin
-
-
-
?
DEVD-FQ + H2O
N2-acetyl-L-lysyl-L-lysyl-L-lysyl-L-arginyl-L-lysyl-L-valyl-beta-alanyl-N6-[[1-([2-[(3E)-3-(2,3-dihydro-1H-indolium-1-ylidene)-6-(2,3-dihydro-1H-indol-1-yl)-3H-xanthen-9-yl]phenyl]sulfonyl)piperidin-4-yl]carbonyl]-L-lysyl-N-[(2R)-2-(carboxymethyl)-3-[[(2S)-1-[[(1S)-1,2-dicarboxyethyl]amino]-3-methyl-1-oxobutan-2-yl]amino]-3-oxopropyl]-D-phenylalaninamide + L-alanyl-N-[2-[(6-[3,3-dimethyl-2-[(1E,3E,5E)-5-(1,3,3-trimethyl-1,3-dihydro-2H-indol-2-ylidene)penta-1,3-dien-1-yl]-3H-indolium-1-yl]hexanoyl)amino]ethyl]-L-prolinamide
-
highly selective substrate for caspase-3
-
-
?
DEVD-NucView488 + H2O
?
-
the highly cell-permeable caspase-3 substrate is obtained by linking a fluorogenic DNA-binding dye to the caspase-3 recognition sequence that renders the dye nonfunctional. On substrate cleavage, the dye is released and becomes highly fluorescent on binding to DNA. DEVD-NucView488 detects caspase-3 activation within a live-cell population much earlier and with higher sensitivity compared with other apoptosis reagents. Cells incubated with DEVD-NucView488 exhibit no toxicity and normal apoptotic progression. DEVD-NucView488 is an ideal substrate for kinetic studies of caspase-3 activation because it detects caspase-3 activity in real-time and also efficiently labels DNA in nuclei of caspase-3-activated cells for real-time fluorescent visualization of apoptotic morphology
-
-
?
DW3-FQ + H2O
N2-acetyl-L-lysyl-L-lysyl-L-lysyl-L-arginyl-L-lysyl-L-valyl-beta-alanyl-N6-[[1-([2-[(3E)-3-(2,3-dihydro-1H-indolium-1-ylidene)-6-(2,3-dihydro-1H-indol-1-yl)-3H-xanthen-9-yl]phenyl]sulfonyl)piperidin-4-yl]carbonyl]-L-lysyl-N-[(2R)-2-(carboxymethyl)-3-[[(3S)-1-[[(2S)-1-[[(1S)-1,2-dicarboxyethyl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-5-methyl-1-oxohexan-3-yl]amino]-3-oxopropyl]-D-phenylalaninamide + L-alanyl-N-[2-[(6-[3,3-dimethyl-2-[(1E,3E,5E)-5-(1,3,3-trimethyl-1,3-dihydro-2H-indol-2-ylidene)penta-1,3-dien-1-yl]-3H-indolium-1-yl]hexanoyl)amino]ethyl]-L-prolinamide
-
-
-
-
?
glutaredoxin-1 + H2O
?
-
murine or human protein substrate, the putative cleavage site of caspase-3, amino acids 56-59 EFVD and 56-59 AIQD, which has predicted affiffinity toward glutamic and aspartic acid residues
cleavage produces a 8 kDA fragment
-
?
IETD-7-amido-4-fluoromethylcoumarin + H2O
IETD + 7-amino-4-fluoromethylcoumarin
-
-
-
-
?
myeloid cell leukemia 1 + H2O
?
-
i.e. Mcl-1, apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand requires specific cleavage of Mcl-1 at D127 and D157 by enzyme. Removal of N-terminal domain of Mcl-1 by enzyme allows for the maximal mitochondrial perturbation that potentiates apoptosis
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Ala-Pro-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Ala-Val-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Asn-Pro-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Asn-Val-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Glu-Val-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Gly-Pro-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Gly-Val-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Leu-Pro-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Leu-Pro-Asp-N6-[methyl red]-Lys-6-aminohexanoyl-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
the substrate is able to detect and quantify caspase-3 activity in apoptotic cells without cross-reactivity by caspase-7
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Leu-Val-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Val-Pro-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-(5(6)-carboxyfluoresceinyl)-6-aminohexanoyl-Asp-Val-Val-Asp-6-aminohexanoyl-N6-[methyl red]-Lys-[N-(6-aminohexyl)-Gly]8-N2-(6-aminohexyl)-Gly-NH2 + H2O
?
-
-
-
?
N-acetyl-Asp-Glu-Val-Asp-7-amido-4-methylcoumarin + H2O
N-acetyl-Asp-Glu-Val-Asp + 7-amino-4-methylcoumarin
-
-
-
-
?
N-acetyl-Asp-Glu-Val-Asp-7-amido-4-trifluoromethylcoumarin + H2O
N-acetyl-Asp-Glu-Val-Asp + 7-amino-4-trifluoromethylcoumarin
-
-
-
-
?
N-acetyl-DEVD-4-trifluoromethylcoumarin 7-amide + H2O
N-acetyl-DEVD + 7-amino-4-trifluoromethylcoumarin
-
-
-
-
?
N-acetyl-DEVD-7-amido-4-fluoromethylcoumarin + H2O
N-acetyl-DEVD + 7-amino-4-fluoromethylcoumarin
-
-
-
-
?
N-acetyl-DEVD-7-amido-4-methylcoumarin + H2O
N-acetyl-DEVD + 7-amino-4-methylcoumarin
-
-
-
-
?
N-acetyl-L-Asp-L-Glu-L-Val-L-Asp-N'-morpholinecarbonyl-rhodamine 110 + H2O
?
-
cell-permeable substrate, high turnover rate and sensitivity both in enzyme solution and in living cells
-
-
?
N-acetyl-LDEVD-7-amido-4-methylcoumarin + H2O
N-acetyl-LDEVD + 7-amino-4-methylcoumarin
-
-
-
-
?
PAK2 + H2O
?
-
caspase-3 is mainly responsible for the apoptotic cleavage of PAK2 in Fas-stimulated Jurkat cells
-
-
?
pro-caspase-6 + H2O
?
-
caspase-8 activates caspase-3, and caspase-3 in turn activates caspase-6. Caspase 3 has a major role in nuclear apoptosis
-
-
?
pro-interleukin-18 + H2O
IL18 + ?
-
virus infection by influenzy A or Sendai virus induces proteolytic processing of IL-18 in human macrophages via caspase-1 and caspase-3 activation
-
-
?
RelB + H2O
?
-
the Asp205 site in RelB is specifically cleaved by caspase-3 in vinblastine-treated HAT-1080 cells
-
-
?
Rho-GDI 1 + H2O
?
-
differential regulation of the homologous GDP dissociation inhibitors Rho-GDI 1 and D4-GDI during drug-induced apoptosis by proteolysis mediated by caspase-3
-
-
?
sterol regulatory element-binding protein + H2O
?
-
cleavage site is DEPD-/-
-
-
?
19 S proteasome + H2O
?
-
caspase-3 specifically cleaves the 19 S component of 26 S proteasome Rpt2, Rpt6, and Rpn2 in skeletal muscle stimulating proteasome activity
-
-
?
Ac-DEVD-4-nitroanilide + H2O
Ac-DEVD + 4-nitroaniline
an artificial caspase-3 substrate
-
-
?
Ac-DEVD-4-nitroanilide + H2O
Ac-DEVD + 4-nitroaniline
-
-
-
?
Ac-DEVD-7-amido-4-methylcoumarin + H2O
Ac-DEVD + 7-amino-4-methylcoumarin
-
-
-
-
?
Ac-DEVD-7-amido-4-methylcoumarin + H2O
Ac-DEVD + 7-amino-4-methylcoumarin
-
the active site of caspase-3 is located at Cys163, which plays a key role in substrate hydration
-
-
?
acetyl-Asp-Glu-Val-Asp-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-Asp-Glu-Val-Asp + 7-amino-4-trifluoromethylcoumarin
-
-
-
-
?
acetyl-Asp-Glu-Val-Asp-7-amido-4-trifluoromethylcoumarin + H2O
acetyl-Asp-Glu-Val-Asp + 7-amino-4-trifluoromethylcoumarin
-
-
-
-
?
acetyl-Asp-Glu-Val-Asp-p-nitroanilide + H2O
acetyl-Asp-Glu-Val-Asp + p-nitroaniline
-
-
-
-
?
acetyl-Asp-Glu-Val-Asp-p-nitroanilide + H2O
acetyl-Asp-Glu-Val-Asp + p-nitroaniline
-
-
-
-
?
acetyl-DEVD-7-amido-4-methylcoumarin + H2O
acetyl-DEVD + 7-amino-4-methylcoumarin
-
high activity
-
-
?
acetyl-DEVD-7-amido-4-methylcoumarin + H2O
acetyl-DEVD + 7-amino-4-methylcoumarin
-
-
-
-
?
acetyl-DEVD-7-amido-4-methylcoumarin + H2O
acetyl-DEVD + 7-amino-4-methylcoumarin
-
-
-
?
acetyl-DEVD-7-amido-4-methylcoumarin + H2O
acetyl-DEVD + 7-amino-4-methylcoumarin
-
DEVD is the optimal tetrapeptide recognition motif
-
-
?
Asp-Glu-Val-Asp-4-nitroanilide + H2O
Asp-Glu-Val-Asp + 4-nitroaniline
-
caspase-3 specific substrate
-
-
?
Asp-Glu-Val-Asp-4-nitroanilide + H2O
Asp-Glu-Val-Asp + 4-nitroaniline
-
-
-
-
?
beta-N-acetylglucosaminidase + H2O
?
-
cleavage during apoptosis into two fragments during apoptosis, an N-terminal fragment containing the O-GlcNAcase active site and a C-terminal fragment containing a region with homology to GCN5 histone acetyltransferases, mutation D413A abrogates cleavage by caspase-3 both in vitro and in vivo. O-GlcNAcase activity is not affected by caspase-3 cleavage because the N- and C-terminal O-GlcNAcase fragments remain associated after the cleavage
-
-
?
beta-N-acetylglucosaminidase + H2O
?
-
mapping of the celavage site by Edman sequencing, the site is a noncanonical recognition site that occurs after Asp413 of the SVVD sequence in human substrate O-GlcNAcase, mutation D413A abrogates cleavage by caspase-3 both in vitro and in vivo
-
-
?
cytokeratine 18 + H2O
?
-
caspase-induced cytokeratine 18 cleavage in apoptotic cell populations
-
-
?
DEVD-7-amido-4-fluoromethylcoumarin + H2O
DEVD + 7-amino-4-fluoromethylcoumarin
-
-
-
-
?
DEVD-7-amido-4-fluoromethylcoumarin + H2O
DEVD + 7-amino-4-fluoromethylcoumarin
-
-
-
-
?
eIF4G + H2O
?
-
caspase 3 is capable of cleaving eIF4G as part of the translationally active complex eIF4F, thereby inactivating this complex and subsequently causing inhibition of translation in apoptotic cells
-
-
?
ICAD + H2O
?
-
activity of caspase-activated deoxyribonuclease, CAD, is affected by the caspase 3-mediated cleavage of the CAD inhibitor, ICAD
-
-
?
ICAD + H2O
?
-
caspase 3-mediated cleavage of the caspase-activated deoxyribonuclease inhibitor, ICAD
-
-
?
mammalian sterile 20-like kinase 1 + H2O
?
-
i.e. Mst1. Caspase 3 preferentially activates extracellular signal-regulated kinase preferentially through 36000 Da cleaved forms of Mst1. The 36000 Da form of Mst1 selectively phosphorylates extracellular signal-regulated kinase
-
-
?
Mcl-1 + H2O
?
-
antiapoptotic protein. Caspase-3 -mediated Mcl-1 downregulation appears to be responsible for the pro-apoptotic effects of EXEL-0862 on FIP1L1-PDGFRalpha-expressing cells
-
-
?
MDM2 oncoprotein + H2O
?
-
because MDM2 functions as a negative regulator of the p53 tumor suppressor and because p53 induces apoptosis in response to a variety of stimuli, this cleavage of MDM2 by CPP32-like proteases may result in deregulation of p53 and contribute directly to the process of apoptotic cell death
-
-
?
nuclear mitotic apparatus protein + H2O
?
-
cleavage at sites distinct from caspase-6
-
-
?
p65/RelA + H2O
?
-
caspase-3-mediated carboxy-terminal fragment of p65/RelA production, cells producing this truncated p65/RelA do not undergo apoptosis but show a high viability, in spite of caspase-3 activation, overview. The substrate translocate to the nucleus, associates with NF-kappaB1/p50 and IkappaBalpha, but cannot bind -kappaB consensus sites
-
-
?
p65/RelA + H2O
?
-
caspase-3-mediated carboxy-terminal fragment of p65/RelA production, no activity with substrate mutants V91L/D94E, D97E, and D94E/D97E
-
-
?
poly(ADP-ribose) polymerase + H2O
85000 Da fragment + ?
caspase-3 is the predominant poly(ADP-ribose) polymerase cleaving enzyme
-
-
?
poly(ADP-ribose) polymerase + H2O
85000 Da fragment + ?
caspase-3 is the predominant poly(ADP-ribose) polymerase cleaving enzyme
-
-
?
pro-Mch2alpha + H2O
?
-
the enzyme processes pro-Mch2alpha at three aspartate processing sites, Asp23, Asp179, and Asp193, to produce the large p18 and small p11 subunits of the mature Mch2alpha enzyme
-
-
?
pro-Mch2alpha + H2O
?
-
the enzyme processes pro-Mch2alpha at three aspartate processing sites, Asp23, Asp179, and Asp193, to produce the large p18 and small p11 subunits of the mature Mch2alpha enzyme. Mch2alpha is a downstream protease activated in CPP32- and granzyme B-mediated apoptosis
-
-
?
pro-Mch6 + H2O
?
-
the enzyme processes proMch6 preferentially at Asp330 to generate two subunits of molecular masses 37000 Da and 10000 Da
-
-
?
pro-Mch6 + H2O
?
-
the enzyme processes proMch6 preferentially at Asp330 to generate two subunits of molecular masses 37000 Da and 10000 Da. Mch6 is a downstream protease activated in CPP32- and granzyme B-mediated apoptosis
-
-
?
protein kinase Cdelta + H2O
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protein kinase Cdelta plays a major role in the regulation of cell apoptosis and survival. PKCdelta is cleaved by caspase 3 to generate a constitutively active catalytic domain that mediates both its apoptotic and anti-apoptotic effects. The phosphorylation of Tyr332 is necessary for the caspase 3-dependent cleavage of protein kinase Cdelta
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protein kinase Cdelta + H2O
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the phosphorylation of Tyr332 is necessary for the caspase 3-dependent cleavage of protein kinase Cdelta
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protein kinase Czeta + H2O
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major cleavage site EETD-/-G, also cleaves at DGMD-/-G and DSED-/-L
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protein kinase Czeta + H2O
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major cleavage site EETD-/-G, also cleaves at DGMD-/-G and DSED-/-L. Caspase-3 is involved in processing of protein kinase Czeta to carboxyl-terminal fragments that are catalytically active and that are degraded by the ubiquitin-proteasome pathway
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protein phosphatase-1 inhibitor-3 + H2O
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the substrate is an in vivo target of caspase-3 and participates in the apoptotic response to induction by actinomycin D, overview
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protein phosphatase-1 inhibitor-3 + H2O
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recombinant His6-tagged substrate protein expressed in Escherichia coli, substrate mutant D49A is not cleaved by caspase-3
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RFC140 + H2O
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cleavage at three sites: DEVD723G, DLVD922S and IETD1117A
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RFC140 + H2O
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cleavage of RFC140 during apoptosis inactivates its function in DNA replication and generates truncated forms that further inhibit DNA replication
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Rpt5 + H2O
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in myoblasts, Rpt5 is sensitive to caspase-3-induced cleavage but in myotubes, it is not sensitive. Caspase-3 cleavage of Rpt5 is responsible for the difference in the patterns of proteasome subunit cleavage in myoblasts compared with myotubes
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tau protein + H2O
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cleavage by caspase-3 is a crucial upstream event associated with Tau self-assembly leading to Alzheimer's Disease pathogenesis
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tau protein + H2O
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peptides are designed from 441-mer major human Tau protein sequence that encompasses the proposed caspase-3 cleavage site (Asp421-/-Ser422). While the control peptide is efficiently cleaved by caspase-3 at Asp421-/-Ser422 site producing the expected N- and C-terminal fragment peptides, the corresponding phospho-Ser422 peptide remains completely resistant to the cleavage. Substitution of Asp421 by its dextro isoform also blocks peptide cleavage by caspase-3. However substitution of Ser422 by its dextro isoform in the peptide does not affect the cleavage significantly
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transcription factor Pax7 + H2O
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compensatory growth and regeneration of skeletal muscle is dependent on the resident stem cell population, satellite cells (SCs). Self-renewal and maintenance of the SC niche is coordinated by the paired-box transcription factor Pax7. Continued expression of this protein inhibits the myoblast differentiation program. Caspase 3 cleavage inactivation of Pax7 is a crucial step for terminating the self-renewal process
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additional information
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apoptosis is a result of a complex network of signaling pathways initiating from both inside and outside the cell, culminating in the activation of caspases, cyteine aspartate proteases, that execute the final stages of cell death
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additional information
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characterization of 14 natural zebrafish caspase-3 substrates
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additional information
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emodin induces apoptosis through caspase 3-dependent pathway in HK-2 cells
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additional information
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interaction of Hsp27 with the caspase-3 prodomain inhibits the second proteolytic cleavage necessary for caspase-3 activation
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?
additional information
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active caspase-3 is involved in apoptosis in epithelial cells of the intestine
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additional information
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azinomycin epoxide leads to activation and apoptosis in THP-1 cells in a p53-independent manner
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?
additional information
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caspase 3 acts as executioner proteases causing proteolysis of key proteins leading to DNA fragmentation and apoptosis
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additional information
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caspase family proteases are key proteins in apoptotic signaling pathways, which are activated in both the death receptor-mediated and the mitochondria-mediated apoptosis pathways
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additional information
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caspase-3 activation results in apoptosis, ischemic/reperfusion in brain leads to increased release of cytochrome c from mitochondria and activation of caspase-3, ischemic preconditioning and ischemic tolerance can diminish the activation of caspase-3, regulation, overview
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additional information
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caspase-3 has a downstream effector function in apoptosis
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additional information
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caspase-3 is activated by the death receptor pathway leading to apoptosis. Human herpesvirus HHV-6A-induced apoptosis is associated with activation of caspase-8, caspase-9, and caspase-3, suggesting the involvement of death receptor and mitochondrial signaling pathways, overview. HHV-6 differentially influences the functions of naive T cells and different subsets of memory CD4+ and CD8+ T cells, which in part may be due to differential susceptibility to HHV-6A-induced apoptosis, overview
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?
additional information
?
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caspase-3 is an effector caspase. The intrinsic death pathway involves mitochondrial release of cytochrome c, which interacts with Apaf-1 and dATP to promote procaspase-9 autoactivation, which in turn activates downstream effectors such as caspase-3, -6, and -7. Increased caspase-3 activation is involved in apoptosis, inhibition of caspase-8 impairs Leptospira interrogans-induced caspase-3 and -6 activation, as well as PARP and lamin A/C cleavage and apoptosis, overview. Leptospira interrogans-induced apoptosis in macrophages is mediated by caspase-3 and -6 activation through a FADDcaspase-8-dependent pathway, independently of mitochondrial cytochrome ccaspase-9-dependent signaling. Caspase-3 is required for the activation of caspase-6 and seems to be involved in caspase-9 activation through a feedback amplification loop. Regulation, overview
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additional information
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caspase-3 is involved in apoptosis in myeloid leukemia cells, Bcl-2 family proteins are the central regulators of caspases activation, overview
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additional information
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caspase-3 is involved in apoptosis. Follistatin-like 1, FSTL1, induces apoptosis in cancer cells and leads to activation of caspase-3 when transfected to ovarian or endometrial cancer or healthy cells, regulation, overview
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additional information
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caspase-3 is playing a central role in the execution of apoptosis, its activation induces Dox resistance, mechanism, overview
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additional information
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caspase-3, an effector caspase, is involved in MDA-MB-231 apoptotic cell death, overview. Caspase-3 is activated when procaspase-3 is cleaved subsequently from the recruitment of Fas associated protein with death domain, FADD, to the death-effector domain site of procaspase-8 during the oligomerization of death receptor and its ligand
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additional information
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caspase-3, convergent with a variety of death signals, plays a key role in the induction of apoptosis
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additional information
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caspases 3, 8 and 9 are essential to rhein-induced apoptosis, inhibitors of caspases 3, 8 and 9 are efficiently blocked by rhein-induced apoptosis in TNF-alpha-treated human aortic smooth muscle cells, overview
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additional information
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caspases are key effectors in the processes of apoptosis and inflammation, executioner caspases selectively hydrolyze cellular proteins in the pathways leading to cell death
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additional information
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constitutive caspase-3 is one of the downstream effectors of TNF-alpha receptor-1 binding, that increases in parallel with the loss of CD28 in long-term T lymphocyte cultures, but this effect is blunted in the presence of the TNF-alpha inhibitors
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additional information
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external lactic acid induces apoptosis via the caspase-dependent pathway activating caspase-3, -8, and -9, and the caspase-independent pathway causing increased expressions of AIF and EndoG, overview
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additional information
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homocysteine-mediated EPC toxicity is due to apoptosis involving caspase-8, cytochrome c release, and caspase-3 activation. Vitamin B6, and B9 significantly impair homocysteine-mediated EPC caspase-3 activation in vitro, overview
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additional information
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human adenovirus type 5 early region 1A, E1A, significantly inhibits the cell proliferation of HeLa by the apoptosis induction through HER-2/Neu/caspase-3 pathway, overview
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additional information
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hypertonicity-induced cation channels, HICC, inhibition by flufenamate and silencing of alpha-ENaC increases the rate of apoptosis in HepG2 cells via activation of caspase-3 or caspase-7
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additional information
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initial activation of caspase-3 causes degradation of glutaredoxin-1, resulting in S-glutathionylation of Fas at cysteine 294, which subsequently enhances binding of FasL, aggregation of Fas, accumulation of Fas in lipid rafts, DISC assembly, and further activation of caspases, causing a propagation of apoptotic cell death. activation of caspases is required for degradation of glutaredoxin-1 and S-glutathionylation of Fas, engagement of Fas causes a rapid activation of caspase-8. Overexpression of Grx1 prevents increases in S-glutathionylation of Fas and attenuates caspase activation and apoptosis in response to receptor ligation. Cleaved caspase-8 and -3 demonstrate an association between active caspases and Grx1 in cells after ligation of Fas, whereas in control cells, these associations are not observed, regulation, overview
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additional information
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insulin inhibits caspase-3 activity in renal tubular epithelial cells via the PI3-kinase/Akt pathway
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additional information
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lipopeptide-induced apoptosis in MCF-7 cells is associated with caspase-3
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additional information
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mechanisms of plasma free fatty acid-triggered vascular smooth muscle cell-apoptosis essentially include activation of caspase-3, overview
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additional information
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mycotoxin citrinin has a strong impact on the expression levels of diverse proteins including the caspase-3, citrinin-directed caspase 3 activation involves MAPK signaling pathways, overview
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additional information
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netrin-1 siRNA-induced H-358 cell death is mediated by caspase-3 and -9 activities, but not by caspase-8 activity
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additional information
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the apoptotic effect of cisplatin is caspase-dependent. Caspase-3 inhibitors prevent HA14-1-induced apoptosis in follicular lymphoma B cells
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additional information
?
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the extrinsic death receptor pathway of apoptosis proceeding entirely via an intrinsic, Bcl-2-controlled, mitochondrial pathway, does not rely on caspase-9 and requires only limited activation of caspase-3 relative to other chemotherapeutic drugs, overview
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additional information
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TRAIL and TRAIL death receptors form a complex, which transmits an apoptotic signal via the Fas associated death domain leading to activation of caspase-8 or other initiator caspases, which in turn activate downstream caspases, such as caspase-3, 9, 6 and 7, that cause cell death, overview
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?
additional information
?
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caspase-3 recognizes various P4 residues in its numerous protein substrates, Asp is the most frequent P4 residue in peptide substrates. Although a wide variety of P4 residues in the cellular proteins are cleaved by caspase-3. Hydrophobic residues appear in the relative frequency of Val-Ala-Leu-Met-Phe-Ile/Cys in descending order. The P4 residues forms favorable hydrophobic interactions in two separate hydrophobic regions of the binding site. The side chains of P4 Ile and Tyr form hydrophobic interactions with caspase-3 residues Trp206 and Trp214 within a non-polar pocket of the S4 subsite, while P4 Trp interacts with Phe250 and Phe252 that can also form the S5 subsite, adaptability of caspase-3 for binding diverse P4 residues, substrate specificity, overview
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additional information
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caspases contain a reactive cysteine critical for enzymatic activity. Increased S-glutathionylation of Fas, caspase-3 activity, and cell death in cells lacking Grx1
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additional information
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the aspartic acid residue in position P1 is a nearly absolute requirement for the caspase activity, at least three additional amino acids at positions P2 to P4 are required to complete the specificity
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additional information
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apoptosis is triggered through intrinsic mitochondrial pathway by caspase 3-activation involving mitochondrial membrane potential damage and reactive oxygen species production
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additional information
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caspase-3 activity is absent in case of coronary occlusion with and without subsequent revascularization in C57BL6 mice after transient ligation followed by 24 h of reperfusion, or 24 h persistent ligation, overview
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additional information
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caspase-3 activity is involved in cell death, e.g. induced by simulated ischemia and reperfusion with pH playing an important role, overview
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additional information
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caspase-3 is activated during apoptosis, overexpression of bovine growth hormone has antiapoptotic effects in several cell lines, including human colonic adenocarcinoma cells, and in colonic mucosa reducing the activation of caspase-3, molecular mechanisms and regulation, overview
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additional information
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caspase-3 is an effector caspase lying downstream from both intrinsic apoptotic pathway mediators and extrinsic apoptotic pathway mediators
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?
additional information
?
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caspase-3 is an effector caspase. The intrinsic death pathway involves mitochondrial release of cytochrome c, which interacts with Apaf-1 and dATP to promote procaspase-9 autoactivation, which in turn activates downstream effectors such as caspase-3, -6, and -7. Increased caspase-3 activation is involved in apoptosis, inhibition of caspase-8 impairs Leptospira interrogans-induced caspase-3 and -6 activation, as well as PARP and lamin A/C cleavage and apoptosis, overview. Leptospira interrogans-induced apoptosis in macrophages is mediated by caspase-3 and -6 activation through a FADDcaspase-8-dependent pathway, independently of mitochondrial cytochrome ccaspase-9-dependent signaling. Caspase-3 is required for the activation of caspase-6 and seems to be involved in caspase-9 activation through a feedback amplification loop. Regulation, overview
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additional information
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caspase-3 is one of the key executioners of apoptosis and responsible for the partial or total proteolytic cleavage of many proteins. Senescence-accelerated prone mice 8 and senescence-accelerated resistant mice 1 show a drop in age-related proteolytic activity of caspase-3, but the caspase-independent cell death, owing to high p53 and apoptosis-inducing factor levels, might be an alternative pathway of cell death in the aged brain
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additional information
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caspases are a family of cysteine aspartic acid-specific proteases playing an important role in apoptotic processes in mammalian cells. Among them, caspase-3 is an essential protease that degrades other protein substrates inside the cells at an early stage of apoptosis
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additional information
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inotodiol, a lanostane triterpenoid, from Inonotus obliquus, inhibits P388 cell proliferation through caspase-3-dependent apoptosis
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additional information
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nonobese diabetic mouse acinar cells at 16 weeks show increased caspase 3 activity, as well as increased expression of TNF-alpha receptor1, increased Bax, tumour protein 53-induced nuclear protein1alpha, and chromatin condensation, apoptosis patterns, overview
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additional information
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caspase-3 causes chromatin condensation through DNA fragmentation
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additional information
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the caspase-3 cleavage site is present within the ATPase domain of Rpt subunits
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additional information
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caspase-3 is an effector caspase lying downstream from both intrinsic apoptotic pathway mediators and extrinsic apoptotic pathway mediators
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?
additional information
?
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caspase-3 activity is absent in case of coronary occlusion with and without subsequent revascularization in C57BL6 mice after transient ligation followed by 24 h of reperfusion, or 24 h persistent ligation, overview
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?
additional information
?
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caspase-3 activity is involved in cell death, e.g. induced by simulated ischemia and reperfusion with pH playing an important role, overview
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?
additional information
?
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activated caspase-3 in irradiation-induced microglia death. This age-dependent irradiation-induced loss of microglia likely affects both the response to irradiation and further brain development, overview
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additional information
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activation of caspase-3, an executioner caspase, plays a key role in the apoptotic cascade
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additional information
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caspase-3 is involved in apoptosis in thymocytes, enzyme inhibition increases cell survival, regulation, overview
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?
additional information
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caspase-3 is involved in glutamate-induced neuronal cell death, overview
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additional information
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caspase-3 is involved in the ischemic brain injury during experimental stroke. In vitro nitric oxide regulates calpain and caspase-3 activation, and in vivo neuronal nitric oxide synthase, calpain and caspase-3 participate in the ischemic brain injury, inhibition of the neuronal nitric oxide synthase by 7-nitroindazole leads to downregulation of caspase-3, mechanism, overview
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?
additional information
?
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direct activation of procaspase-3 by caspase-9 and caspase-8 in type I cells, radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis additionally requires changes upstream of caspase-8 activation, regulation of caspase-8 and apoptosis in hepatocytes, overview. Irradiation induces TNF-alpha-mediated activation of caspase-8, -9, and -3, and apoptosis in hepatocytes. Apoptosis induction is prevented by IkappaB antisense oligonucleotides mediated by suppression of caspases-9 and -3 activation but not of caspase-8 activation, overview
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?
additional information
?
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enzyme regulation in response to damaging agents like ethanol and acetylsalicylic acid in gastric mucosa, overview
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?
additional information
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increased cytosolic cytochrome c and subsequently caspase-3 activation are additional signs of neuronal death via the mitochondrial pathway. Bradykinin administration significantly attenuates ischemia-induced neuronal death, and also suppresses the release of MnSOD, and cytochrome c, and prevents caspase-3 activation
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additional information
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N-methyl-D-aspartate induces the activation of caspase-3 and the caspase-3-dependent apoptotic pathway, the activation is prevented by the autocamtide-2-related inhibitory peptide, overview. Blockade of calcium/calmodulin-dependent protein kinase II-alpha activity prevents N-methyl-D-aspartate-induced caspase-3 activation and provides significant neuroprotection against N-methyl-D-aspartate-induced ganglion cell loss in a retina toxicity model
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additional information
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T-cells show activated caspase-3 with the preservation of photoreceptors
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?
additional information
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procaspase-3 is activated by caspase-9 and caspase-8
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pre-interleukin-1beta + H2O
additional information
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-
a 28000 Da fragement and a 17000 Da fragement, less efficient hydrolysis than with caspase-1
?
pre-interleukin-1beta + H2O
additional information
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-
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a 28000 Da fragement and a 17000 Da fragement, less efficient hydrolysis than with caspase-1
?
pre-interleukin-1beta + H2O
additional information
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a 28000 Da fragement and a 17000 Da fragement, less efficient hydrolysis than with caspase-1
?
