Nanopublications

Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RAlJqV3PalxRr2oMplIUfaMKDNrauGEgfJKTM6KM5qMvo#provenance>. }

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_5 label "Selventa" provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
large_corpus.bel version "20131211" provenance.
large_corpus.bel authoredBy _5 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _4 provenance.
assertion hadPrimarySource 15322527 provenance.
_4 wasQuotedFrom 15322527 provenance.
_4 value "Figure 2 | Extrinsic and intrinsic apoptotic signalling pathways in neurons. Black lines represent apoptotic pathways, blue lines represent survival pathways. The extrinsic death pathway is initiated by binding of the extracellular ligands, TNFa (tumour necrosis factor-a) or FAS (apoptosis antigen-1) ligand (FASL), to death receptors TNFR1 (TNF-receptor1) and FAS. TNFR1 activation leads to the formation of a TRADD RIP TRAF2 (TNF receptor death domain receptor interacting protein TNF associated factor 2) complex, which signals through the NFkB (nuclear factorkB) survival pathway (blue lines) or the JNK (cJun N teminal kinase)death pathway (black lines). RIP activates procaspase 2 and cleaves BID (BH3 (BCL2 (B-cell leukaemia/lymphoma-2) homology domain 3) interacting agonist). The TRADD FADD FLICE (TNF receptor death domain FAS associated death domain FADD like interleukin 1b) complex activates procaspase 8, triggering apoptosis through caspase 3 or cleavage of BID to tBID (truncated BID). FAS-mediated death occurs through a FADD-mediated activation of procaspase 8 or DAXX (death-associated protein )-mediated activation of JNK. JNK modifies BID to jBID, allowing its translocation to the mitochondrion and release of SMAC/DIABLO (second-mitochondrialderived activator of caspases). The intrinsic apoptotic pathway is initiated at the mitochondrion by diverse stimuli. Membrane permeabilization is mediated by BH3-only proteins, which sequester and inhibit the supression of BAX (B-cell lymphoma 2-associated protein X) by BCL2, allowing mitochondrial BAX translocation and the release of cytochrome c (Cyto c), SMAC/DIABLO, AIF (apoptosis-inducing factor) and HTRA2/OMI (high temperature requirement serine protease 2)." provenance.