| Literature DB >> 11387339 |
L M McAllister-Lucas1, N Inohara, P C Lucas, J Ruland, A Benito, Q Li, S Chen, F F Chen, S Yamaoka, I M Verma, T W Mak, G Núñez.
Abstract
Bcl10 and MALT1, products of distinct chromosomal translocations in mucosa-associated lymphoid tissue lymphoma, cooperate in activating NF-kappaB. Mice lacking Bcl10 demonstrate severe immunodeficiency associated with failure of lymphocytes to activate nuclear factor kappaB (NF-kappaB) in response to antigen receptor stimulation and protein kinase C activation. We characterize Bimp1, a new signaling protein that binds Bcl10 and activates NF-kappaB. Bimp1-mediated NF-kappaB activation requires Bcl10 and IkappaB kinases, indicating that Bimp1 acts upstream of these mediators. Bimp1, Bcl10, and MALT1 form a ternary complex, with Bcl10 bridging the Bimp1/MALT1 interaction. A dominant negative Bimp1 mutant inhibits NF-kappaB activation by anti-CD3 ligation, phorbol ester, and protein kinase C expression. These results suggest that Bimp1 links surface receptor stimulation and protein kinase C activation to Bcl10/MALT1, thus leading to NF-kappaB induction.Entities:
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Year: 2001 PMID: 11387339 DOI: 10.1074/jbc.M103824200
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157