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Details on Person In the absence of BAFFR (TNFSF13C) ligation to BAFF (TNFSF13...

Class:IdSummation:5676258
_displayNameIn the absence of BAFFR (TNFSF13C) ligation to BAFF (TNFSF13...
_timestamp2015-02-19 18:33:39
created[InstanceEdit:5676482] Garapati, Phani Vijay, 2015-02-19
literatureReference[LiteratureReference:5668503] Nonredundant and complementary functions of TRAF2 and TRAF3 in a ubiquitination cascade that activates NIK-dependent alternative NF-kappaB signaling
[LiteratureReference:5668419] Noncanonical NF-kappaB activation requires coordinated assembly of a regulatory complex of the adaptors cIAP1, cIAP2, TRAF2 and TRAF3 and the kinase NIK
textIn the absence of BAFFR (TNFSF13C) ligation to BAFF (TNFSF13B) ligand, NFkB-inducing kinase (NIK) forms a complex with TNF receptor associated factor 3 (TRAF3) and TRAF2 which exists in a preassembled complex with cellular Inhibitor of apoptosis 1 (cIAP1) and cIAP2 in the cytosol. cIAP1/2 targets NIK for degradation by ubiquitylation, there by inhibiting non-canonical NFkB pathway (Vallabhapurapu et al. 2008, Zarnegar et al. 2008). Upon BAFF trimer binding to BAFFR, TRAF3 but not TRAF2 is recruited to the receptor via a 'PVPAT' binding site. This unique feature of BAFFR to recruit TRAF3 instead of TRAF2 is primarily due to its possession of an atypical TRAF-binding sequence (Morrison et al 2005). Following recruitment to BAFFR, TRAF3 undergoes proteasomal degradation, a process which requires TRAF2 and cIAP1/2.
(summation)[Reaction:5676596] TRAF3 binds BAFFR:BAFF [Homo sapiens]
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