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CASP12 — CASP2

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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