◀ Back to CASP8
CASP8 — TNFRSF1A
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
CASP8
→
TNFRSF1A
(increases, TNFRSF1A Activity, CASP8 Activity)
Zheng et al., Mol Cell Biol 2006*
Evidence: We found that TRADD is required for TNFR1 to induce NF-kappaB activation and caspase-8-dependent apoptosis but is dispensable for TNFR1-initiated, RIP1-dependent necrosis.
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OpenBEL Selventa BEL large corpus:
CASP8
→
Complex of TNF-TNFRSF1A
(increases, TNF/TNFRSF1A Activity)
Evidence: protein kinase C (PKC) modulator byrostatin induces myeloid leukemia cell lines to produce TNF, resulting in autocrine engagement of TNF-receptors and apoptosis induction through a mechanism that is suppressible by TNFR-Fc fusion protein and caspase-8 dominant-negative (Cartee et al.,2002)
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BioCarta tnfr1 signaling pathway:
TNF-alpha/TNF R1/RIP/RAIDD/MADD/TRADD/TRAF2/cIAP complex (TNF-CRADD-TRAF2-BIRC3-TNFRSF1A-MADD-RIPK1-TRADD)
→
FADD/Caspase 8 complex (CASP8-FADD)
(modification, activates)
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BioCarta tnfr1 signaling pathway:
TNF-alpha/TNF R1/RIP/RAIDD/MADD/TRADD/TRAF2/cIAP complex (TNF-CRADD-TRAF2-BIRC3-TNFRSF1A-MADD-RIPK1-TRADD)
→
Caspase 8 (CASP8)
(modification, activates)
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BioCarta ceramide signaling pathway:
FADD/Caspase 8 complex (CASP8-FADD)
→
TNF/TNF R/TRADD/MADD/cIAP/RIP/TRAF2/RAIDD complex (TRADD-MADD-BIRC3-RIPK1-TRAF2-CRADD-TNFRSF1A-TNF)
(modification, collaborate)
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KEGG Toxoplasmosis:
TNFRSF1A
→
CASP8
(protein-protein, activation)
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NCI Pathway Database HIV-1 Nef: Negative effector of Fas and TNF-alpha:
TNFR1A/Caspase 2/TNF-alpha/FADD/TRADD/RIP/cIAP2/TRAF1/TRAF2/Ask1/RAIDD complex (TNFRSF1A-CASP2-TNF-FADD-TRADD-RIPK1-MAP3K5-TRAF1-TRAF2-BIRC3-CRADD)
→
FAS/FADD/DAXX/Ask1/Caspase 8/Caspase 8/FASLG complex (FASLG-CASP8-MAP3K5-FAS-DAXX-FADD)
(modification, activates)
Micheau et al., Cell 2003, Yang et al., Cell 1997, Saitoh et al., EMBO J 1998, Chang et al., Science 1998
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NCI Pathway Database Ceramide signaling pathway:
FADD/Caspase 8 complex (CASP8-FADD)
→
TNF-alpha/TNFR1A/TRADD/MADD/cIAP2/RIP/TRAF2/RAIDD complex (TRADD-MADD-BIRC3-RIPK1-TRAF2-CRADD-TNFRSF1A-TNF)
(modification, collaborate)
Boldin et al., Cell 1996, Muzio et al., Cell 1996
Evidence: assay
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NCI Pathway Database Caspase Cascade in Apoptosis:
sTNF-alpha/TNFR1A/TRADD/TRAF2/FADD complex (TNFRSF1A-TRADD-TRAF2-FADD-TNF)
→
Caspase 8 (CASP8)
(modification, activates)
Bodmer et al., Nat Cell Biol 2000, Sprick et al., Immunity 2000, Schneider-Brachert et al., Immunity 2004, Schneider-Brachert et al., J Clin Invest 2006, Lavrik et al., J Biol Chem 2008, Boldin et al., Cell 1996, Walczak et al., EMBO J 1997, Scaffidi et al., EMBO J 1998
Evidence: mutant phenotype, assay, physical interaction
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NCI Pathway Database TNF receptor signaling pathway :
sTNF-alpha/TNFR1A/TRADD/TRAF2/FADD complex (TNFRSF1A-TRADD-TRAF2-FADD-TNF)
→
Caspase 8 (CASP8)
(modification, activates)
Schneider-Brachert et al., Immunity 2004, Schneider-Brachert et al., J Clin Invest 2006, Boldin et al., Cell 1996
Evidence: mutant phenotype, assay, physical interaction
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NCI Pathway Database TNF receptor signaling pathway :
sTNF-alpha/TNFR1A/TRADD/TRAF2/FADD complex (TNFRSF1A-TRADD-TRAF2-FADD-TNF)
→
Caspase 8 (tetramer) complex (CASP8)
(modification, activates)
Schneider-Brachert et al., Immunity 2004, Schneider-Brachert et al., J Clin Invest 2006, Boldin et al., Cell 1996
Evidence: mutant phenotype, assay, physical interaction
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NCI Pathway Database TNF receptor signaling pathway :
Caspase 8 (CASP8)
→
sTNF-alpha/TNFR1A/TRADD/RIP/TRAF2/cIAP1/cIAP2 complex (TNFRSF1A-TRADD-RIPK1-TRAF2-BIRC2-BIRC3-TNF)
(modification, collaborate)
Schneider-Brachert et al., Immunity 2004, Schneider-Brachert et al., J Clin Invest 2006, Boldin et al., Cell 1996
Evidence: mutant phenotype, assay, physical interaction
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NCI Pathway Database TNF receptor signaling pathway :
sTNF-alpha/TNFR1A/TRADD/RIP/TRAF2/cIAP1/cIAP2 complex (TNFRSF1A-TRADD-RIPK1-TRAF2-BIRC2-BIRC3-TNF)
→
Caspase 8 (tetramer) complex (CASP8)
(modification, inhibits)
Schneider-Brachert et al., Immunity 2004, Schneider-Brachert et al., J Clin Invest 2006, Boldin et al., Cell 1996
Evidence: mutant phenotype, assay, physical interaction
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WikiPathways Nanoparticle triggered regulated necrosis:
TNFRSF1A
→
RIPK1/FADD/TRADD/CASP8/RIPK3
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Estellés et al., Dev Biol 1999
:
The phosphoprotein protein PEA-15 inhibits Fas- but increases
TNF-R1 mediated
caspase-8 activity and apoptosis
Yin et al., J Mol Med (Berl) 2000
:
Bid is a novel pro-apoptosis Bcl-2 family protein that is activated by
Caspase 8 in
response to
Fas/TNF-R1 death receptor activation
Yin et al., Cell Res 2000
(Liver Diseases) :
Bid is a novel pro-apoptosis Bcl-2 family protein that is activated by
caspase 8 in
response to
Fas/TNF-R1 death receptor signals
Fotin-Mleczek et al., J Cell Sci 2002
(Rhabdomyosarcoma) :
Apoptotic crosstalk of TNF receptors : TNF-R2-induces depletion of TRAF2 and IAP proteins and accelerates
TNF-R1 dependent
activation of
caspase-8 ... Compared with FasL induced cell death
TNF-R1 induced activation of
caspase-8 was significantly weaker and delayed ... Thus, TNF-R2 may compete with TNF-R1 for the recruitment of newly synthesized TRAF2 bound anti-apoptotic factors, thereby promoting the formation of a
caspase-8 activating
TNF-R1 complex
Chau et al., Nat Cell Biol 2002
(Shock, Septic) :
Correspondingly, the release of cytochrome c and the activation of
caspase-3 induced by
TNFRI , but not by DNA damage, are defective in cells expressing Rb-MI
Wang et al., Mol Cell Biol 2004
:
The pX-dependent expression of Fas/FasL and
TNFR1/TNF-alpha mediates
caspase 8 activation, resulting in Bid cleavage
Guthmann et al., Respir Res 2005
(Hyperoxia) :
In the initiation phase of pulmonary oxygen toxicity, an increase of TNFalpha and its receptor
TNFR1 leads to the activation of
caspase 8 and 3 in TIIcells
Kilpatrick et al., J Leukoc Biol 2006
(MAP Kinase Signaling System) :
delta-PKC associates with
TNFR-1 in response to TNF and is
required for NFkappaB activation and inhibition of
caspase 3
Van Themsche et al., Endocrinology 2008
(Carcinoma...) :
On the opposite, TNFalpha up-regulated XIAP in Hec-1A cells ; in these cells, the cytokine induced delayed
TNF-R1 dependent activation of
caspase-8 , and failed to activate caspases -9 and -3 and to induce apoptosis
White et al., Am J Physiol Lung Cell Mol Physiol 2012
(Acute Kidney Injury...) :
We further elucidated pathways of
TNFR1 mediated apoptosis with NF-?B ( Complex I ) and
caspase-8 ( Complex II ) expression and discovered that TNFR1 proapoptotic signaling induces NF-?B activation
White et al., Shock 2012
(Acute Kidney Injury...) :
Ischemic AKI drives distinct proinflammatory and proapoptotic changes in the pulmonary EC transcriptome with
TNFR1 dependent
caspase activation and programmed cell death
Kofod-Olsen et al., J Virol 2012
:
Here, we report that infection by human herpesvirus 6B ( HHV-6B ) inhibited poly ( ADP-ribose ) polymerase ( PARP ) cleavage,
caspase 3 and 8
activation , and I?Ba Ser-32 phosphorylation downstream of
TNFR1 , indicating inhibition of both the inflammatory and apoptotic signaling pathways
Mizrahi et al., Stem Cells 2013
:
Progenitor stimulation is selectively mediated by
TNF-R1 and
involves activation of
caspase-8 , without redundant activity of TNF-R2
Hu et al., J Biol Chem 1997
:
In this report, we describe the cloning and characterization of
I-FLICE , a novel
inhibitor of
tumor necrosis factor receptor-1- and CD-95 induced apoptosis
Srinivasan et al., J Biol Chem 1998
(Breast Neoplasms) :
Thus, at least in some cells,
caspase-8 signaling in
response to Fas or
TNFR1 stimulation is regulated by a Bcl-xL-inhibitable step
Nguyen et al., J Biol Chem 1998
:
This contrasts with the anti-apoptotic influence of Bcl-2 family proteins in the cell death pathway induced by Fas ligand or tumor necrosis factor (TNF), in which Bcl-2 typically acts downstream of
Fas/TNFR1 mediated activation of
caspase-8 ... Moreover, E1A induces procaspase-8 processing and cell death in cells deleted of FADD, an adaptor protein critical for
Fas/TNFR1 activation of
caspase-8