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CASP12 — CASP2
Text-mined interactions from Literome
Kilic et al., Cell Death Differ 2002
:
Formation of noncanonical high molecular weight
caspase-3 and -6 complexes and
activation of
caspase-12 during serum starvation induced apoptosis in AKR-2B mouse fibroblasts
Feng et al., Am J Physiol Gastrointest Liver Physiol 2002
(Necrosis) :
Caspase-3 was activated in primary hepatocytes by STS treatment, but
caspase-9 and -12 were not
activated , and
caspase-3 activation is not dependent on caspase-8
Morishima et al., J Biol Chem 2002
:
Cytochrome c-independent
activation of
caspase-9 by
caspase-12 ... These results suggest that
caspase-12 can
activate caspase-9 without involvement of cytochrome c
Chan et al., Neurobiol Dis 2002
(Alzheimer Disease) :
Moreover,
activation of
caspase-12 , an endoplasmic reticulum ( ER ) -associated
caspase , is greatly increased in cells expressing mutant PS1
Justo et al., J Am Soc Nephrol 2003
:
Caspase-2 , caspase-3, and caspase-9 were activated, and specific
caspase inhibitor
prevented apoptosis and increased long-term survival
Fu et al., Cardiovasc Res 2004
:
Caspase-2 , -3, -6 and -9 were activated during apoptosis and
caspase-2 inhibitor ( Z-VDVAD-FMK ) and caspase-3 inhibitor ( Z-DEVD-FMK ) significantly
attenuated the apoptosis
Perchellet et al., Anticancer Drugs 2004
:
Caspase-2 and -8 may both act upstream of mitochondria to promote Cyt c release, but
caspase-2 is already maximally
activated 6 h after 4 microM DAU or TT13 treatments, whereas DAU- or TT-induced caspase-8 and -9 activities peak at 9 h. Pre-treatments with 15 microM of the caspase-2 inhibitor benzyloxycarbonyl ( z ) -Val-Asp-Val-Ala-Asp ( VDVAD ) -fluoromethyl ketone ( fmk ) totally block DAU- and TT13 induced caspase-2, -8 and -9 activities, whereas pre-treatments with 15 microM of the caspase-8 inhibitor z-Ile-Glu-Thr-Asp ( IETD ) -fmk prevent DAU and TT13 from inducing caspase-8 activities without affecting their caspase-2- and -9-inducing activities, suggesting that the induction of apical caspase-2 activity by these drugs may be a critical upstream event required for the activation of other downstream caspases, including caspase-9 and the mitochondrial amplification loop through caspase-8
Aoyama et al., J Cereb Blood Flow Metab 2005
(Acidosis) :
Acidosis also increased caspase-12 mRNA expression, caspase-12 protein expression, cleavage of
caspase-12 to its active form, and
activation of
caspase-3
Ho et al., FEBS J 2005
:
Caspase-2 is resistant to inhibition by inhibitor of apoptosis proteins ( IAPs ) and can
activate caspase-7
Obeng et al., J Biol Chem 2005
:
We further demonstrate that ER stress induced apoptosis is a caspase dependent process that does not require the expression of
caspase-12 or caspase-4 but can be
inhibited by overexpression of Bcl-x ( L ) or a dominant negative
caspase-9
Lombard et al., Leuk Res 2005
(Leukemia, T-Cell) :
Caspase-2 inhibitor
blocked THC induced
caspase-3 in wild-type Jurkat cells but not loss of Deltapsi ( m )
Nakano et al., Cardiovasc Res 2006
:
A non-selective
caspase inhibitor, z-VAD.fmk ( 100 microM ),
inhibited apoptosis and cleavage of
caspase-12 stimulated by thapsigargin, while a calpain inhibitor, MDL 28170 ( 120 microM ), inhibited caspase-12 cleavage but not apoptosis
Cervia et al., Apoptosis 2006
(Pituitary Neoplasms) :
In addition, we provide evidence that euplotin C treatment results in rapid activation of ryanodine receptors, depletion of Ca2+ stores in the endoplasmic reticulum ( ER ), the release of cytochrome c from the mitochondria,
activation of
caspase-12 , and activation of
caspase-3 , leading to apoptosis
Kumar et al., Cardiovasc Res 2007
(Acidosis...) :
Simulated ischemia had no significant effect on caspase-8 cleavage, but induced cleavage of
caspase-3 and caspase-12 and led to a slight release of cytochrome C. Prevention of cytosolic acidosis ( anoxia at pH ( o ) 7.4 ) had no effect on cytochrome C release, but significantly reduced apoptosis, attenuated cytosolic Ca2+ overload, and
prevented cleavage of
caspase-12
Fábián et al., J Virol 2007
(Carcinoma...) :
While
caspase-8 and caspase-9 are not involved in MTH-68/H induced apoptosis, activation of caspase-3 and
caspase-12 was
detected in virus infected PC12 cells
Lin et al., Biochem Biophys Res Commun 2007
(Spinocerebellar Ataxias) :
PKCgamma SCA14 mutant proteins were shown to cause aggregation which initially resulted in endoplasmic reticulum ( ER ) stress and cell apoptosis as demonstrated by phosphorylation of PERK on Thr981,
activation of
caspase-12 , increases in BiP/GRP78 protein levels, and consequent activation of
caspase-3
Park et al., Biochem Pharmacol 2011
:
Further analysis using selective caspase inhibitors revealed that
caspase-12 activation was
required for activation of
caspase-9 and -3 to the sufficient level for subsequent activation of caspase-7 and -8
Stefanis et al., J Neurochem 1997
:
We have shown previously that selective
cysteine aspartase ( caspase ) inhibitors protect PC12 cells and sympathetic neurons from such death, and that the caspase
Nedd-2 is
required for this type of death to occur