Gene interactions and pathways from curated databases and text-mining

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CASP3 — CASP8

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Sun et al., Oncogene 1999 (Adenocarcinoma...) : The caspase inhibitors ( Z-DEVD-FMK and Z-VAD-FMK ) suppressed CD437 induced CPP32-like caspase activation and apoptosis in both cell lines
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
Selznick et al., J Neuropathol Exp Neurol 2000 : Caspase-3 deficiency, or pharmacological inhibition of caspase activity, prevented caspase-3 activation and blocked the appearance of apoptotic nuclear features but not Abeta induced neuronal death
Nakatsuka et al., Neurosci Lett 2000 (Ischemic Attack, Transient) : Although pro-caspase-3 was strongly detected, active caspase-3 was not detected before and until 84 h after 5-min ischemia
Okamoto et al., Rheumatology (Oxford) 2000 (Arthritis, Rheumatoid) : Caspase-8-specific inhibitor suppressed the activation of caspase-3 after Fas ligation on RA synoviocytes
De Saint Jean et al., Invest Ophthalmol Vis Sci 2000 : Apoptosis was confirmed by a cleavage of PARP and CPP32 , by caspase-8 activation , and by an index Hoechst/neutral red greater than one
Zhang et al., J Neurosci 2000 (Alzheimer Disease) : Caspase-3 induces neuronal apoptosis in 20 % of the cells, whereas caspase-7 or -8 do not induce apoptosis
Tomicic et al., Biochem Biophys Res Commun 2001 : Caspase-3- and caspase-9 mediated cleavage of Bcl-2 was efficiently blocked by caspase-3 ( zDEVD ) and caspase-9 ( zLEHD ) inhibitor, respectively
Kagawa et al., Clin Cancer Res 2001 : Caspase-3 deficiency, however, did not affect Bax induced levels of poly ( ADP-ribose ) polymerase cleavage, caspase-6 activation, and lamin B cleavage
Kumi-Diaka et al., Biol Cell 2000 (Carcinoma...) : The major findings of these studies are : i ) genistein inhibits growth and proliferation of both LNCaP and DU145 cells via apoptosis mainly, and necrosis at higher concentrations ; ii ) genistein induces activation and expression of caspase-3 ( CPP32 ) in both target cells ; iii ) genistein induced apoptosis and CPP32 activation could be significantly inhibited by the caspase-3 inhibitor, z-VAD-fmk ( N-benzyloxycarbonyl-Val-Asp-fluoromethyl-ketone ), thus confirming a mediator role of CPP32 in the genistein induced apoptotic pathway in the target cells
Stadelman et al., Brain Pathol 2001 (Fetal Death...) : Expression of apoptosis associated proteins p53, bcl-2, bax, and caspase-3/CPP32 , activation of caspase-3 , and modification of proteins via poly ( ADP-ribosyl ) ation was studied in pontosubicular neuron necrosis ( PSN ), a form of perinatal brain damage revealing the morphological hallmarks of neuronal apoptosis
Hernandez et al., Surgery 2001 (Colonic Neoplasms) : Western blots were performed to assess intracellular expression of Flice-like inhibitory protein (FLIP) , a caspase inhibitor
Kwon et al., Exp Mol Med 2002 : Caspase-3 selective inhibitor, Ac-DEVD-CHO, prevented both the activation of caspase-3 and cleavage of poly ( ADP-ribose ) polymerase ( PARP )
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
Chandra et al., J Biol Chem 2003 : Here we present evidence that the mitochondrially localized active caspase-9 and -3 result mostly from translocation from the cytosol ( into the intermembrane space ) and partly from caspase mediated activation in the organelle rather than from the Apaf-1 mediated activation
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 ... 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
Schoemaker et al., J Hepatol 2003 (Cholestasis...) : Apoptosis was determined by TUNEL staining, active caspase-3 staining, activation of caspase-8 , -9 and -3
Aouad et al., J Immunol 2004 : Caspase-3 is a component of Fas death inducing signaling complex in lipid rafts and its activity is required for complete caspase-8 activation during Fas mediated cell death
Yang et al., Nephron. Experimental nephrology 2004 (Necrosis) : Here we evaluate three caspase inhibitors : B-D-FMK ( pan caspase inhibitor ), Z-DEVDFMK ( predominantly Caspase-3 inhibitor ) and Z-VAD-FMK ( predominantly Caspase-1 and -3 inhibitor ) to ameliorate apoptosis induced by cisplatin in rat proximal tubular ( RPT ) cells
Kusunoki et al., BMC pharmacology 2004 (Arthritis, Rheumatoid) : Caspase-3 activity was increased by treatment with triptolide and was suppressed by caspase inhibitors
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
Liszewska et al., Prostaglandins Other Lipid Mediat 2005 : Treatment of luteal cells with P4 and PGE2 for 24 h decreased ( P < 0.05 ) level of active caspase-3 while aminoglutethimide ( P < 0.05 ), spermine NONOate ( P < 0.05 ), and staurosporine ( P < 0.001 ) increased caspase-3 activity in the cells
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
Shankar et al., J Neurosci 2006 : Rhgas6 and caspase inhibitors also reduced active caspase-3 immunoreactivity relative to TNFalpha-only treated cultures
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
Nakadai et al., Toxicology 2006 : Chlorpyrifos also induced an increase of intracellular active caspase-3 in U937 cells in a dose dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, significantly inhibited the chlorpyrifos induced apoptosis
Yang et al., Apoptosis 2006 : Caspase-3 mediated-feedback and activation of caspase-8 and -9 in MCF-7/C3 cells is further supported by an increase in the cleavage of caspase-8 and 9 substrates and cytochrome c release
Koo et al., Am J Chin Med 2007 : Caspase-3 activation and subsequent apoptotic cell death in MGG treated cells were partially blocked by the caspase-3 inhibitor, Z-DEVD-FMK
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
Ikeda et al., Exp Cell Res 2007 : Caspase-3 activation is also induced, but the caspase inhibitor, Z-VAD-FMK, does not block RASSF6 mediated apoptosis
Wong et al., Biochim Biophys Acta 2007 : Caspase-3 is activated by cleavage of caspase-8 and caspase-9
Denault et al., Biochem J 2007 : Caspase 3 attenuates XIAP ( X-linked inhibitor of apoptosis protein ) -mediated inhibition of caspase 9
Feng et al., J Huazhong Univ Sci Technolog Med Sci 2007 : Caspase-3 inhibitors can suppress caspase-3 activity and reduce the apoptosis rate significantly
Li et al., Toxicology 2007 : DDVP also induced an increase of intracellular active caspase-3 in NK-92CI in a dose- and time dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, significantly inhibited DDVP induced apoptosis, suggesting that this apoptosis is partially mediated by activation of intracellular caspase-3
Wei et al., Zhonghua Xue Ye Xue Za Zhi 2007 : The caspase-3 activity was markedly enhanced, and the active caspase-3 in K562/ADM cells increased by about 40 % compared to liposome alone and non silencing controls
Audo et al., Arthritis Res Ther 2007 (Arthritis, Rheumatoid) : Caspase 3 , a key mediator of apoptosis, was not activated in celecoxib treated RA FLSs, and the presence of specific caspase 3 or pan-caspase inhibitors did not affect celecoxib induced cell death
Scarlatti et al., Cell Death Differ 2008 (Breast Neoplasms) : Here we show that resveratrol arrests cell proliferation, triggers death and decreases the number of colonies of cells that are sensitive to caspase-3 dependent apoptosis ( MCF-7 casp-3 ) and also those that are unresponsive to it ( MCF-7vc )
Li et al., Toxicology 2009 : Chlorpyrifos also induced an increase in intracellular active caspase-3 in Jurkat T cells in a dose- and time dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, significantly inhibited chlorpyrifos induced apoptosis
Liang et al., Zhonghua Yu Fang Yi Xue Za Zhi 2008 : p, p'-DDE, beta-BHC and their mixture could induce the apoptosis of Sertoli cells in vitro which was associated with activation of Caspase-3 mediated by cleavage of Caspase-8 and Caspase-9
Tang et al., Oncol Rep 2009 (Adenocarcinoma...) : Caspase-9 and -3 inhibitors almost completely suppressed HCT induced caspase-9 and -3 activities
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
Li et al., Arch Toxicol 2011 (Necrosis) : DNA fragmentation was detected when cells were treated with 0.5, 1, or 2 µM ziram for 24 h. Ziram also induced an increase in intracellular active caspase-3 in U937 cells in a dose dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, significantly inhibited the ziram induced apoptosis
Xiao et al., Apoptosis 2011 : Caspase-3 activity was 10-fold higher in myotubes compared to myoblasts, and Stsp caused a significant caspase-3 induction in both
Jeyasuria et al., Biol Reprod 2011 : The IAP family members are the only endogenous inhibitors of active caspase 3 , and MCL1 limits activation of caspase 3 by suppressing proapoptotic signaling
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
Aras et al., Brain Res 2012 (Gliosis) : Reactive neonatal and adult astrocytes demonstrated an increase in total caspase activity with a corresponding increase in the expression of active caspase-3 in the absence of cell death
Edgington et al., Chem Biol 2012 : We also demonstrate that caspase-6 activation does not require active caspase-3/-7 , suggesting that it may autoactivate or be cleaved by other proteases
Nelson et al., Crit Care Med 2012 (Muscular Atrophy) : These findings support our hypothesis that a regulatory calpain/caspase-3 cross-talk exists whereby calpain can promote caspase-3 activation and active caspase-3 can enhance calpain activity in diaphragm muscle during prolonged mechanical ventilation
Chan et al., J Virol 2012 : However, HCMV infection does induce a temporal activation of caspase 3, with only a low level of active caspase 3 being observed after the 48-h viability checkpoint
Wu et al., Food Chem Toxicol 2013 : Caspase-3 inhibitor also efficiently blocked CD95 ( APO-1/CD95 ) and Bax expression, caspase-3 activation and PARP cleavage, whereas antioxidant N-acetyl-l-cysteine, AMPK inhibitor and AMPK siRNA effectively blocked the AMPK phosphorylation
Wright et al., J Exp Med 1997 (Lymphoma) : Only the caspase inhibitors, however, prevented activation of CPP32-like activity as revealed by cleavage of the synthetic substrate, DEVD-pNa, by cell cytosols, and also by in vivo cleavage of poly ( ADP-ribosyl ) polymerase, a known substrate of CPP32
Deveraux et al., EMBO J 1998 : In contrast, these IAP family proteins did not prevent caspase-8 induced proteolytic activation of pro-caspase-3 ; however, they subsequently inhibited active caspase-3 directly, thus blocking downstream apoptotic events such as further activation of caspases
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