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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAdv95inWS_HuMcKBTW1ny4431SaXS6Q55RUAMUGWulnM#_7 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAdv95inWS_HuMcKBTW1ny4431SaXS6Q55RUAMUGWulnM#_6 http://www.w3.org/ns/prov#value IAP, inhibitor of apoptosis; SMAC, second mitochondria-derived activator of caspase. In the death receptor pathway, ligands such as tumour-necrosis factor (TNF), FAS ligand (also known as CD95L), or TNF-related apoptosis-inducing ligand (TRAIL, also known as APO2 ligand (APO2L) or TNF ligand superfamily member 10 (TNFSF10)) interact with their respective death receptors (TNF receptor 1 (TNFR1), FAS (also known as CD95) and death receptor 4 (DR4, also known as TRAIL receptor 1 (TRAILR1)) or DR5 (also known as TRAILR2), respectively). These interactions ultimately lead to the recruitment of the FAS-associated death domain (FADD) and the activation of the protease caspase 8. 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