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CASP12 — CASP8

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Zhuang et al., Exp Cell Res 1999 : Caspase-8 mediates caspase-3 activation and cytochrome c release during singlet oxygen induced apoptosis of HL-60 cells
Raoul et al., J Cell Biol 1999 : Motoneurons resistant to Fas activation expressed high levels of FLICE-inhibitory protein (FLIP) , an endogenous inhibitor of caspase-8 activation
Okamoto et al., Rheumatology (Oxford) 2000 (Arthritis, Rheumatoid) : Caspase-8-specific inhibitor suppressed the activation of caspase-3 after Fas ligation on RA synoviocytes
Hernandez et al., Surgery 2001 (Colonic Neoplasms) : Western blots were performed to assess intracellular expression of Flice-like inhibitory protein (FLIP) , a caspase inhibitor
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
Thomas et al., Surgery 2002 (Pancreatic Neoplasms) : FLICE-like inhibitory protein (FLIP) , an inhibitor of caspase-8 , ( also known as FLICE ) is regulated by the transcription factor nuclear factor-kappaB (NF-kappaB) and can contribute to TRAIL resistance
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
Xu et al., Anticancer Res 2003 (Pancreatic Neoplasms) : Caspase-8 and -3 activities were increased by TRAIL treatment and apoptosis was largely blocked by caspase-8 and -3 inhibitors
Fujii et al., Infect Immun 2003 : Caspase-8 is known to activate Bid, and a specific inhibitor of caspase-8 prevented the mitochondrial damage
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
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
Maitra et al., Crit Care Med 2005 (Sepsis) : Caspase-8 activates caspase-3 , which in turn degrades fibronectin and focal adhesion kinase and leads to disruption of hepatic architecture and integrity
Miyao et al., Otol Neurotol 2006 (Cholesteatoma, Middle Ear) : Caspase-8 , which is activated by the induction of tumor necrosis factor-alpha, leads to activation of caspase-3 , which activates apoptotic nucleases
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
Wu et al., Cell Mol Life Sci 2006 : Caspase-8 played important roles in the activation of caspase-3 and induction of apoptosis, whereas the role of the caspase-9 was limited
Yamaguchi et al., Biochim Biophys Acta 2006 (Carcinoma, Hepatocellular...) : We demonstrated that Adv-Casp8 increased expression of active forms of caspase-8 in MOI dependent manner
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
Faragher et al., Mol Biol Cell 2007 (Breast Neoplasms) : Caspase-8 activates cytoplasmic caspase-7 , which is likely to be the primary caspase responsible for cleavage of CENP-C and INCENP, a key chromosomal passenger protein
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
Pesakhov et al., Nutr Cancer 2010 (Leukemia, Myeloid, Acute) : Caspase-8 inhibition abrogated Bid cleavage and strongly reduced caspase-9 activation, suggesting that the cross-talk mechanism mediated by caspase-8 dependent Bid cleavage can contribute to the activation of the intrinsic apoptotic pathway by curcumin + carnosic acid
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
Moujalled et al., Cell Death Differ 2012 : In mouse embryonic fibroblasts, neither caspase-8 nor cellular FLICE-inhibitory protein (FLIP) is necessary for TNF to activate NF-?B, but caspase-8 is required for TNF to cause cell death, and induction of FLIP by NF-?B is required to prevent it
Sata et al., J Biol Chem 1998 : Here, we show that endothelial cell apoptosis by OxLDL and LPC-C16 : 0 was dose dependent and correlated with down-regulation of FLICE-inhibitory protein (FLIP) , an intracellular caspase inhibitor
Yamashita et al., Blood 1999 : Caspase-8 activated caspase-3 and T18 in neutrophil cytoplasmic extracts