Noncanonical NF-κB activation requires coordinated assembly of a regulatory complex of the adaptors cIAP1, cIAP2, TRAF2 and TRAF3 and the ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2008-12

AUTHORS

Brian J. Zarnegar, Yaya Wang, Douglas J. Mahoney, Paul W. Dempsey, Herman H. Cheung, Jeannie He, Travis Shiba, Xiaolu Yang, Wen-chen Yeh, Tak W. Mak, Robert G. Korneluk, Genhong Cheng

ABSTRACT

Recent studies suggest that nuclear factor kappaB-inducing kinase (NIK) is suppressed through constitutive proteasome-mediated degradation regulated by TRAF2, TRAF3 and cIAP1 or cIAP2. Here we demonstrated that the degradation of NIK occurs upon assembly of a regulatory complex through TRAF3 recruitment of NIK and TRAF2 recruitment of cIAP1 and cIAP2. In contrast to TRAF2 and TRAF3, cIAP1 and cIAP2 seem to play redundant roles in the degradation of NIK, as inhibition of both cIAPs was required for noncanonical NF-kappaB activation and increased survival and proliferation of primary B lymphocytes. Furthermore, the lethality of TRAF3 deficiency in mice could be rescued by a single NIK gene, highlighting the importance of tightly regulated NIK. More... »

PAGES

1371-1378

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni.1676

DOI

http://dx.doi.org/10.1038/ni.1676

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1053487240

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18997794


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