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Ferch, U.* ; Meyer zum Büschenfelde, C.* ; Gewies, A.* ; Wegener, E. ; Rauser, S. ; Peschel, C.* ; Krappmann, D. ; Ruland, J.*

MALT1 directs B cell receptor–induced canonical nuclear factor-kappaB signaling selectively to the c-Rel subunit.

Nat. Immunol. 8, 984-991 (2007)
DOI PMC
NF-kappaB (Rel) transcription factors control physiological and pathological immune cell function. The scaffold proteins Bcl-10 and MALT1 couple antigen-receptor signals to the canonical NF-kappaB pathway and are pivotal in lymphomagenesis. Here we found that Bcl-10 and MALT1 differentially regulated B cell receptor–induced activation of RelA and c-Rel. Bcl-10 was essential for recruitment of the kinase IKK into lipid rafts for the activation of RelA and c-Rel, for blocking apoptosis and for inducing division after B cell receptor ligation. In contrast, MALT1 participated in survival signaling but was not involved in IKK recruitment or activation and was dispensable for RelA induction and proliferation. MALT1 selectively activated c-Rel to control a distinct subprogram. Our results provide mechanistic insights into B cell receptor–induced survival and proliferation signals and demonstrate the selective control of c-Rel in the canonical NF-kappaB pathway.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
ISSN (print) / ISBN 1529-2908
e-ISSN 1529-2916
Journal Nature Immunology
Quellenangaben Volume: 8, Issue: 9, Pages: 984-991 Article Number: , Supplement: ,
Publisher Nature Publishing Group
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Research Unit Signaling and Translation (SAT)
Institute of Pathology (PATH)