Statements in which the resource exists.
SubjectPredicateObjectContext
http://www.reactome.org/bio...rdf:typebiopax3:Pathwaylld:biopax3
http://www.reactome.org/bio...biopax3:commentReviewed: Gillespie, ME, 2010-11-30lld:biopax3
http://www.reactome.org/bio...biopax3:commentReviewed: Gay, NJ, 2006-04-24 16:48:17lld:biopax3
http://www.reactome.org/bio...biopax3:commentAuthored: de Bono, B, 2005-08-16 10:54:15lld:biopax3
http://www.reactome.org/bio...biopax3:commentThe first known downstream component of TLR4 and TLR2 signaling is the adaptor MyD88. Another adapter MyD88-adaptor-like (Mal; also known as TIR-domain-containing adaptor protein or TIRAP) has also been described for TLR4 and TLR2 signaling. MyD88 comprises an N-terminal Death Domain (DD) and a C-terminal TIR, whereas Mal lacks the DD. The TIR homotypic interactions bring adapters into contact with the activated TLRs, whereas the DD modules recruit serine/threonine kinases such as interleukin-1-receptor-associated kinase (IRAK). Recruitment of these protein kinases is accompanied by phosphorylation, which in turn results in the interaction of IRAKs with TNF-receptor-associated factor 6 (TRAF6). The oligomerization of TRAF6 activates TAK-1, a member of the MAP 3-kinase family, and this leads to the activation of the IkB kinases. These kinases, in turn, phosphorylate IkB, leading to its proteolytic degradation and the translocation of NF-kB to the nucleus. Concomitantly, members of the activator protein-1 (AP-1) transcription factor family, Jun and Fos, are activated, and both AP-1 transcription factors and NF-kB are required for cytokine production, which in turn produces downstream inflammatory effects.lld:biopax3
http://www.reactome.org/bio...biopax3:commentEdited: Shamovsky, V, 2012-04-19lld:biopax3
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