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CASP4 — CASP8
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
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
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
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
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
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
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
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
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