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FAS — TNFRSF1A

Pathways - manually collected, often from reviews:

• 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
• NCI Pathway Database Caspase Cascade in Apoptosis: sTNF-alpha/TNFR1A/TRADD/TRAF2/FADD complex (TNFRSF1A-TRADD-TRAF2-FADD-TNF) → FASLG/FAS (trimer)/FADD/FADD complex (FAS-FASLG-FADD) (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

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: TNFRSF1A — FAS (association, biochemical) Gajate et al., J Biol Chem 2005

Text-mined interactions from Literome

Quintana et al., J Neurosci Res 2005 (Brain Injuries...) : Lack of TNFR1 signaling also affected the expression of apoptosis/cell death related genes ( Fas , Rip, p53 ), matrix metalloproteinases ( MMP3, MMP9, MMP12 ), and their inhibitors ( TIMP1 ), suggesting a role of TNFR1 in extracellular matrix remodeling after injury
Saqr et al., J Neuropathol Exp Neurol 2006 (Glioma) : We report here that death receptor-5 (DR5), tumor necrosis factor receptor-1 ( TNF-R1 ), and Fas receptor (FasR) are all located in the caveolin-1 enriched membrane fractions, and TRAIL caused the translocation of DR5, FasR, and TNF-R1 to the caveolar fractions
Chauhan et al., Anticancer Drugs 2007 : The Fas-Fas ligand interaction between macrophages and L929 cells increased the expression of Fas associated death domain, and tumor necrosis factor-tumor necrosis factor receptor 1 interaction between macrophages and L929 cells increased the expression of tumor necrosis factor receptor associated death domain in L929 cells
Wosik et al., J Neurol Sci 2007 : TNFR1 ligation induces NFkappaB activation and the upregulation of chemokines MCP-1 and IL-8, as well as adhesion molecules ICAM-1 and VCAM-1, while Fas and DR5 triggering activate the extracellular signal regulated kinases-1 and -2 ( Erk 1/2, p42/44 MAPK ) inducing the release of matrix metalloproteinase 9 (MMP9) by BBB derived ECs
Krogerus et al., Transpl Immunol 2008 (Cytomegalovirus Infections) : CMV enhanced development of CAN was associated with tubular apoptosis and concomitant increase of TNF-alpha-TNF-R1 , rather than the FAS-FAS-ligand activation
Guazzone et al., Microsc Res Tech 2009 (Inflammation...) : Germ cells expressing TNFR1, IL-6R, and Fas increase in number and undergo apoptosis, through the TNF-alpha/TNFR1 , IL-6/IL-6R, and Fas/Fas L systems
Nagafuji et al., Blood 1995 : The TNF-alpha induced Fas expression is mediated by p55 TNF-alpha receptor
Nagafuji et al., Nihon rinsho. Japanese journal of clinical medicine 1996 : The TNF-alpha induced Fas expression is mediated by p55-TNF-alpha receptor
Nagafuji et al., Leukemia & lymphoma 1996 : TNF-alpha induced Fas expression was mediated by p55-TNF-alpha receptor