TRAF2:cIAP1/2 complex binds FN14:TWEAK

Stable Identifier
R-HSA-5676598
Type
Reaction [binding]
Species
Homo sapiens
Compartment
ReviewStatus
5/5
Locations in the PathwayBrowser
General
SVG |   | PPTX  | SBGN
Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout
The FN14 (TNFRSF12A) intracellular domain lacks the characteristic death domain of TNF receptor superfamily (TNFRSF) but contains TNFR-associated factor (TRAF) binding sites. Upon TWEAK binding, FN14 recruits TRAF2 and TRAF3 to activate both canonical and non-canonical nuclear factor-kappa B (NF-kB) pathway (Brown et al. 2003, Saitoh et al. 2003, Sanz et al. 2010). NF-kB activation plays a key role in TWEAK-elicited inflammatory responses. TWEAK/FN14 binding induces NIK activation through targeting the degradation of TRAF2/cellular inhibitor of apoptosis (cIAP) 1 and 2 complex (Vince et al. 2008). TWEAK activation of the non-canonical NF-kB pathways promotes inflammatory responses in tubular cells. In cultured renal tubular cells TWEAK increases nuclear RelB/p52 accumulation, RelB and p52 DNA-binding activity, and NIK- and RelB-dependent CCL21 and CCL19 expression (Poveda et al. 2010).
Literature References
PubMed ID Title Journal Year
12529173 The Fn14 cytoplasmic tail binds tumour-necrosis-factor-receptor-associated factors 1, 2, 3 and 5 and mediates nuclear factor-kappaB activation

Richards, CM, Feng, SL, Winkles, JA, Brown, SA, Hanscom, HN

Biochem. J. 2003
Participants
Participates
Orthologous Events
Authored
Reviewed
Created
Cite Us!