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CASP8 — CYCS

Text-mined interactions from Literome

Tafani et al., Am J Pathol 2000 : Cytochrome c-dependent activation of caspase-3 by tumor necrosis factor requires induction of the mitochondrial permeability transition
Livne et al., J Virol 2001 : Cytochrome c is released into the cytosol in E4orf4 expressing cells, but caspase-9 is not required for induction of apoptosis
Joseph et al., Oncogene 2001 (Carcinoma, Non-Small-Cell Lung...) : Cytochrome c release, activation of caspase-9 and the executioner caspase-3 were observed in both types of lung cancer cells
Segal et al., Am J Physiol Cell Physiol 2001 : Cytochrome c-mediated activation of caspase-3 is the final common pathway for most signals that induce apoptosis
Osawa et al., Liver 2001 : Cytochrome c release and caspase-9 activation are required for the activation of executor caspase-3 in TNF-alpha induced hepatocyte apoptosis, but caspases-8 and -2 play, if any, a minimal role
Pan et al., J Clin Endocrinol Metab 2001 (Thyroid Neoplasms) : Cytochrome c release was not affected by the inhibitors of caspase-9 , caspase-8 and caspase-3
Henshall et al., Cell Death Differ 2001 (Seizures) : In this study we examine the in vivo formation of the Apaf-1/cytochrome c complex and activation of caspase-9 following limbic seizures in the rat ... These data suggest seizures induce formation of the Apaf-1/cytochrome c complex prior to caspase-9 activation and caspase-9 may be a potential therapeutic target in the treatment of brain injury associated with seizures
Waterhouse et al., Biochimie 2002 : Cytochrome c is involved in apoptosome formation and caspase activation, SMAC/Diablo deregulates the inhibitor of apoptosis proteins, apoptosis inducing factor may play a role in chromatin condensation and release of other proteins such as adenylate kinase may adversely affect cellular metabolism and contribute to the death of a cell if the downstream apoptotic pathway is blocked
Morishima et al., J Biol Chem 2002 : Cytochrome c-independent activation of caspase-9 by caspase-12
Maeda et al., Mol Pathol 2002 (Helicobacter Infections...) : Cytochrome c release from mitochondria was observed and was not inhibited by caspase-8 inhibitor
McGinnis et al., Neurochem Int 2003 (Neuroblastoma) : Cytochrome c translocation does not lead to caspase activation in maitotoxin treated SH-SY5Y neuroblastoma cells
Borutaite et al., FEBS Lett 2003 (Myocardial Ischemia...) : Cytochrome c release can result in caspase activation and thus apoptosis, but also results in mitochondrial dysfunction, which might contribute to contractile dysfunction or necrosis at reperfusion
Zhu et al., Brain Res 2004 (Brain Infarction...) : Cytochrome c release and activation of caspase-3 and -2 at 24 h post-HI were significantly diminished by hypothermia
Ryan et al., J Biochem Mol Toxicol 2004 : Cytochrome c together with Apaf-1 causes activation of the initiator caspase , caspase-9, which in turn activates caspase-3 ultimately leading to the degradation of poly ( ADP-ribose ) polymerase ( PARP )
Lee et al., Stroke 2004 (Cerebral Infarction...) : Cytochrome c release and the activation of caspase-3 were analyzed by Western blotting and immunohistochemistry
Soto-Cerrato et al., Biochem Pharmacol 2004 (Breast Neoplasms) : Cytochrome c release, activation of caspases-9, -8 and -7 and cleavage of poly ( ADP-ribose ) polymerase protein typified the apoptotic event and caspase inhibition revealed that PG acts via the mitochondrial pathway
Vindis et al., Arterioscler Thromb Vasc Biol 2005 (Arteriosclerosis) : Cytochrome C release in turn induced caspase-3 activation
Wang et al., Cancer Res 2005 (Nasopharyngeal Neoplasms) : Cytochrome c in turn activated caspase-9 and caspase-3
Lin et al., World J Gastroenterol 2006 (Stomach Neoplasms) : Berberine induces p53 expression and leads to the decrease of the mitochondrial membrane potential, Cytochrome C release and activation of caspase-3 for the induction of apoptosis
Tyagi et al., J Cell Biochem 2006 (Hyperhomocysteinemia) : Cytochrome-c release contributes to caspase activation, such as caspase-9, caspase-6, and caspase-3, which results in the degradation of numerous nuclear proteins including poly ( ADP-ribose ) polymerase ( PARP ), which subsequently leads to the internucleosomal cleavage of DNA, resulting cell death
Borutaite et al., J Biol Chem 2007 : Cytochrome c release from mitochondria induces caspase activation in cytosols ; however, it is unclear whether the redox state of cytosolic cytochrome c can regulate caspase activation
Chung et al., Proteomics 2007 (Leukemia, Experimental) : Proteomic analysis showed that the altered proteins include the significant regulation of HSP70, chaperonin, ATP synthase beta chains, and Chain F. Western blotting and immuno-cytochemistry stain showed that YC-1 treatment caused a time dependent increase in cytosolic Cytochrome c , pro-caspase-9, Apaf-1, and the activation of caspase-9 and -3
Li et al., Ann Surg Oncol 2009 (Colonic Neoplasms) : Cytochrome c resulted in the activation of caspase-3 , thus activating PARP
Walsh et al., Int J Cancer 2009 (Anoxia...) : This effect is associated with the altered expression of a number of pro- and anti-apoptotic proteins, which leads to inhibition of Cytochrome c release and downstream caspase activation
Bhattacharya et al., Biochem Pharmacol 2010 : Cytochrome c release was followed by the activation of caspase-9, caspase-3 and caspase-7 , and cleavage of PARP in both MOLT-3 and K562 cells
Ye et al., Biol Trace Elem Res 2013 : Cytochrome c (Cyt c) and apoptosis inducing factor release, Bax translocation, collapse of mitochondria membrane potential, caspase 3 and 8 activation, and Bid cleavage were observed along with a sustained activation of extracellular signal regulated kinase ( ERK ) and c-Jun NH2 terminal kinase (JNK)