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CASP1 — 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
Sung et al., PloS one 2013
(Spinal Cord Injuries) :
We show that
p45 forms a complex with FADD and
diminishes Fas-FADD mediated death signaling
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