Bcl10 plays a critical role in NF-κB activation induced by G protein-couple receptors

Donghai Wang, Yun You, Pei Chun Lin, Liquan Xue, Stephan W. Morris, Hu Zeng, Renren Wen, Xin Lin

Research output: Contribution to journalArticle

72 Scopus citations

Abstract

G protein-coupled receptors (GPCRs) play pivotal roles in cell proliferation, differentiation, and survival. Although many studies indicate that the stimulation of GPCRs leads to NF-κB activation, the molecular mechanism by which GPCRs induced NF-κB activation remains largely unknown. Bcl10 is an essential adaptor molecule connecting antigen receptor signaling cascades to NF-κB activation in lymphocytes. However, the function of Bcl10 in nonlymphoid cells remains to be determined. In this study, we demonstrated that the deficiency of Bcl10 resulted in the defect in NF-κB activation induced by either expressing the constitutively active mutant of G protein or stimulation of cells with lysophosphatidic acid or endothelin-1, which activate their GPCR. In contrast, TNF-α-, LPS-, and integrin-induced NF-κB activation was not affected in Bcl10-deficient cells. Together, our results provide genetic evidence showing that Bcl10 is a key signaling component mediating NF-κB activation induced by GPCRs in nonlymphoid cells.

Original languageEnglish (US)
Pages (from-to)145-150
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume104
Issue number1
DOIs
StatePublished - Jan 2 2007

Keywords

  • Endothelin-1
  • Lysophosphatidic acid
  • Signal transduction

ASJC Scopus subject areas

  • General

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