NDLI: Bcl10 plays a critical role in NF-κB activation induced by G protein-coupled receptors

Content Provider	PubMed Central
Author	Wang, Donghai You, Yun Lin, Pei-chun Xue, Liquan Morris, Stephan W. Zeng, Hu Wen, Renren Lin, Xin
Copyright Year	2006
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.
Related Links	http://dx.doi.org/10.1073/pnas.0601894104
Ending Page	150
Page Count	6
Starting Page	145
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	1
Volume Number	104
Language	English
Publisher	National Academy of Sciences
Publisher Date	2007-01-02
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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