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CASP4 — FADD

Text-mined interactions from Literome

Kataoka et al., Curr Biol 2000 : Activation of Fas ( CD95 ) by its ligand ( FasL ) rapidly induces cell death through recruitment and activation of caspase-8 via the adaptor protein Fas associated death domain protein ( FADD )
Kischkel et al., Immunity 2000 (Lymphoma, B-Cell) : Apo2L/TRAIL induced homomeric and heteromeric complexes of DR4 and DR5 and stimulated recruitment of FADD and caspase-8 and caspase-8 activation in nontransfected cells
Gil et al., Oncogene 2000 : The interferon induced protein kinase ( PKR ), triggers apoptosis through FADD mediated activation of caspase 8 in a manner independent of Fas and TNF-alpha receptors
Gil et al., Apoptosis 2000 : The pathway of PKR induced apoptosis involves FADD activation of caspase 8 by a mechanism independent of Fas and TNFR
Morgan et al., Cell Death Differ 2001 (Prostatic Neoplasms) : FADD-DN induces caspase activation in normal epithelial cells as demonstrated using a Fluorescence Resonance Energy Transfer assay that measures caspase activity in individual living cells
Gupta et al., Exp Gerontol 2002 (Lymphopenia) : There was an increased expression of FADD and increased activation of caspase 8 and caspase 3 in lymphocytes from aged humans as compared to young subjects
Yuan et al., Oncogene 2002 (Prostatic Neoplasms) : Since in death receptor signaling, FADD mediates activation of caspase-8 , which in turn cleaves BID, and since caspase-8 is activated in PTEN mediated apoptosis, we examined BID cleavage in PTEN mediated apoptosis
Milner et al., Cell Death Differ 2002 (Ovarian Neoplasms) : Induction of apoptosis by chemotherapeutic drugs : the role of FADD in activation of caspase-8 and synergy with death receptor ligands in ovarian carcinoma cells
Guseva et al., Prostate 2002 (Prostatic Neoplasms) : As predicted, overexpression of FADD-DN prevented activation of caspase-8 and Bid cleavage and attenuated the release of cytochrome c and activation of caspases -2, -7, and -9 ... Overexpression of FADD-DN and Bcl-2 affected the activation of caspase-3 and PARP cleavage differently : FADD-DN attenuated the activation of caspase-3 and PARP cleavage whereas Bcl-2 overexpression prevented caspase-3 activation and completely blocked cleavage of PARP
Rokhlin et al., Prostate 2002 (Prostatic Neoplasms) : Transfection of FADD-DN in LNCaP resulted in inhibition of caspase activation as well as in resistance to combined treatment with TRAIL and wortmannin
Chao et al., J Biol Chem 2002 : In contrast, adenoviral expression of FADD-wt increased apoptosis and caspase-3 activity in CMs under both normoxic and hypoxic conditions ... Surprisingly, FADD-dn , as well as the specific caspase-8 inhibitor benzyloxycarbonyl-IETD-fluoromethylketone also inhibited the activation of caspase-9 and -3 in CMs subjected to hypoxia/SD
Uno et al., Blood 2003 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive...) : Fas associated death domain protein ( FADD ) and caspase-8, components of death inducing signaling complex ( DISC ), as well as FLIP ( FLICE [ Fas associating protein with death domain-like interleukin-1 converting enzyme ] /caspase-8 inhibitory protein ), a negative regulator of caspase-8 , were expressed ubiquitously in Ph1 positive leukemia cell lines irrespective of their differential sensitivities to TRAIL and FasL
Jimbo et al., Exp Cell Res 2003 : The dominant negative form of FADD and z-VAD-fmk inhibited caspase-8 , caspase-9, Bid processing, cytochrome c release, and DNA fragmentation induced by ER stress, suggesting that caspase-8 and caspase-9 are the main caspases involved in ER stress mediated apoptosis of P19-36/12 ( - ) cells
Storey et al., J Biol Chem 2003 : Kv1.3 stimulation required the expression of Fas associated death domain protein and activation of caspase 8, but did not require activation of caspase 3 or protein synthesis
Karlsson et al., J Neurooncol 2004 (Glioma) : The results were consistent with a block in the apoptotic signaling pathways of glioma cells between caspase-8 and caspase-3 activation, and that inducible Fadd could induce caspase-8 independent apoptosis in some cells
Gniadecki et al., Biochem Biophys Res Commun 2004 : We report here that disruption of lipid rafts by cholesterol depleting compounds ( methyl-beta-cyclodextrin, filipin III, cholesterol oxidase, and mevastatin ) leads to a spontaneous clustering of Fas in the non-raft compartment of the plasma membrane, formation of Fas-FADD complexes, activation of caspase-8 , and apoptosis
Chandra et al., Mol Cell Biol 2004 : Functional analyses with dominant negative mutants, small interfering RNAs, peptide inhibitors, and Fas associated death domain (FADD)- and caspase 8-deficient Jurkat T cells establish that the mitochondrion localized active caspase 8 results mainly from the FADD dependent and tumor necrosis factor receptor associated death domain dependent mechanisms and that caspase 8 activation plays a causal role in VP16 induced caspase 3 activation and cell death
Manabe et al., J Reprod Dev 2004 : ( 3 ) FADD activates an initiator caspase ( procaspase-8 ; also called FLICE ), which is a bipartite molecule, containing an N-terminal death effector domain ( DED ) and a C-terminal DD. ( 4 ) Procaspase-8 begins auto-proteolytic cleavage and activation
Rudner et al., Oncogene 2005 : Death receptor induced apoptosis is paradigmatically mediated via the recruitment of FADD adapter molecule to the ligand/receptor complex and subsequent activation of caspase-8
Bender et al., Cell Death Differ 2005 : Cytoplasmic TRADD activates apoptosis through Fas associated death domain protein ( FADD ) and caspase-8 activation that was blocked by caspase inhibitors or dominant negative FADD
Fulda et al., Eur J Cancer 2005 : While resveratrol enhanced TRAIL induced apoptosis through G1 cell cycle arrest and survivin depletion, resveratrol failed to sensitise cells with high expression levels of Bcl-2 or FADD-DN. Interestingly, overexpression of Bcl-2 or FADD-DN did not interfere with resveratrol mediated cell cycle arrest or survivin depletion, but blocked release of cytochrome c and Smac from mitochondria into the cytosol, enhanced caspase activation and apoptosis upon combined treatment with resveratrol and TRAIL indicating that overexpression of Bcl-2 or FADD-DN decoupled the effect of resveratrol on the cell cycle and apoptosis
Ou et al., Hum Immunol 2005 : FADD-DN inhibited caspase-8 activation induced by TRAIL in the transfectants of CM and NES2Y cells
Christgen et al., Cancer Lett 2005 (Pancreatic Neoplasms) : This study investigates the role of caspase-8 and DN-FADD , an inhibitor of CD95 dependent caspase-8 activation, in gemcitabine induced apoptosis of Colo357 pancreatic cancer cells
Alaoui-El-Azher et al., Cell Microbiol 2006 : However, blocking the FasR-FasL interaction by antagonistic antibodies to FasR or to FasL had no effect on P. aeruginosa induced caspase 8 and caspase 3 activation, neither did the silencing of FasR by small interfering RNA ( siRNA ), suggesting that caspase 8 activation through the FADD bypasses FasR/FasL mediated signalling ... Thus, FADD mediated caspase 8 activation involves intracellular ExoS in an ADPRT dependent manner
Cagnol et al., Apoptosis 2006 : However using RNA interference and ectopic expression, we demonstrated that neither FADD nor Fas were necessary for caspase 8 activation and cell death
Li et al., J Cell Physiol 2006 : Expression of dominant negative FADD efficiently prevented OxLDL induced apoptosis and caspase-8 activation
Walczak et al., Methods Mol Biol 2008 : For the CD95 and the TRAIL-R1/R2 DISCs, it is now clear that the adaptor protein Fas associated DD protein (FADD) forms part of these complexes and is necessary for recruitment of the proapoptotic signaling molecules caspase-8 and caspase-10
Zhang et al., Apoptosis 2008 : The change in FADD levels and distribution was dependent on caspase-3 , caspase-8 activity and the presence of BID
Lesinski et al., Cancer Res 2008 (Carcinoma, Renal Cell...) : These data suggest that bortezomib and IFN-alpha act through the extrinsic pathway of apoptosis via FADD induced caspase-8 activation to initiate cell death
Jani et al., Cell Res 2009 (Leukemia, T-Cell) : Inhibition of MAT II and the resultant decrease in SAMe levels enhanced expression of FasL mRNA and protein, and induced DISC ( Death Inducing Signaling Complex ) formation with FADD ( Fas associated Death Domain ) and procaspase-8 recruitment, as well as concomitant increase in caspase-8 activation and decrease in c-FLIP ( s ) levels
Ho et al., J Neurosci 2009 : This pathway is activated by disease triggering mutations, which enhance the LRRK2-FADD association and the consequent recruitment and activation of caspase-8
Hasegawa et al., J Immunol 2009 : ASC mediated AP-1 activation was inhibited by chemical or protein inhibitors for caspase-8, caspase-8 targeting small interfering RNA, and p38 and JNK inhibitors, but not by a caspase-1 inhibitor, caspase-9 or Fas associated death domain protein ( FADD ) dominant negative mutants, FADD- or RICK targeting small interfering RNAs, or a MEK inhibitor, indicating that the ASC induced AP-1 activation is mediated by caspase-8, p38, and JNK, but does not require caspase-1 , caspase-9, FADD, RICK, or ERK
Föger et al., FEBS J 2009 (Burkitt Lymphoma) : This inducible nuclear-cytoplasmic translocation of FADD is independent of CD95 internalization, formation of the death inducing signaling complex, and caspase-8 activation
George et al., J Neurosci Res 2010 (Neuroblastoma) : Genistein triggered the receptor mediated apoptotic pathway through upregulation of TNF-alpha, FasL, TRADD, and FADD and activation of caspase-8
Sodhi et al., Toxicol Mech Methods 2004 : UVB ( 100 mJ/cm ( 2 ) ) irradiation induced apoptosis in macrophages concurrent with expression of Fas, Fas ligand, Fas associated death domain (FADD) , activation of caspase-8 , -3 and cleavage of poly ( ADP-ribose ) polymerase ( PARP )
Shakibaei et al., Antioxid Redox Signal 2010 : Overall, our results indicated that mitochondrial changes are early events in TNF-alpha induced apoptosis and that these mitochondrial changes require recruitment of FADD and caspase-8 activation , but not caspase-3 activation or RIP recruitment
Lokeshwar et al., Cancer Res 2010 (Neoplasm Invasiveness...) : 4-MU induced caspase-8, caspase-9, and caspase-3 activation , PARP cleavage, upregulation of Fas-L, Fas, FADD and DR4, and downregulation of bcl-2, phosphorylated bad, bcl-XL, phosphorylated Akt, phosphorylated IKB, phosphorylated ErbB2, and phosphorylated epidermal growth factor receptor
Liu et al., J Biol Chem 2010 : FADD down-regulation neither restored viability of PILP-1 treated cells nor attenuated production of active caspase-8 and t-Bid in PILP-1 treated cells, suggesting that the death receptor mediated pathway was not involved in the cytotoxicity of PILP-1
Basit et al., J Biol Chem 2012 (Rhabdomyosarcoma) : Importantly, knockdown of RIP1 by RNA interference prevented the formation of the RIP1·FADD·caspase-8 complex and inhibited subsequent activation of caspase-8 , -9, and -3 ; loss of mitochondrial membrane potential ; and apoptosis upon treatment with IAP inhibitor and lexatumumab
Ahmad et al., Cancer Res 1997 : FADD engagement of caspase-8 presumably activates this caspase and leads to apoptosis
Eberstadt et al., Nature 1998 : FADD then activates caspase 8 ( also known as FLICE or MACH ) through an interaction between the death-effector domains of FADD and caspase 8
Faubion et al., J Clin Invest 1999 : Collectively, these data suggest that GCDC induced hepatocyte apoptosis involves ligand independent oligomerization of Fas, recruitment of FADD , activation of caspase 8, and subsequent activation of effector proteases, including downstream caspases and cathepsin B