Please use this identifier to cite or link to this item: http://hdl.handle.net/1783.1/6245

Regulation of transcription factors by heterotrimeric G proteins

Authors Ho, Maurice K.C. HKUST affiliated (currently or previously)
Su, Yan HKUST affiliated (currently or previously)
Yeung, Wing Shan HKUST affiliated (currently or previously)
Wong, Yung Hou View this author's profile
Issue Date 2009
Source Current Molecular Pharmacology , v. 2, (1), 2009, p. 19-31
Summary Lessons from viral hijacks of cells and cancer biology suggest that the activation of G protein-coupled receptors (GPCRs) often results in the modulation of various transcription factors and cofactors. Since drugs acting on GPCRs represent a significant portion of therapeutic agents currently in use, it is important to understand the actions of GPCRs on gene expression. GPCRs and their associated heterotrimeric G proteins are known to regulate gene transcription through complex signaling networks. The G protein-mediated signaling cascades have been extensively studied and accumulating evidence indicates that the four subfamilies of G proteins may utilize both common and unique pathways for transcriptional regulation. This review aims to provide a contemporary account of our understanding on the regulation of transcription factors by GPCRs, with a special emphasis on specific regulations of transcription factors such as STAT3 and NF-κB by individual G protein subfamilies. Functional impacts of the signal integration between different pathways and the contributions by other GPCR-interacting molecules will also be briefly discussed. © 2009 Bentham Science Publishers Ltd.
Subjects
ISSN 1874-4672
Rights We would like to give credit to Bentham Science Publishers for granting us permission to repost this article.
Language English
Format Article
Access View full-text via DOI
View full-text via Scopus
Find@HKUST
Files in this item:
File Description Size Format
HoetalRegulationoftranscriptionfactorsbyGPCRrevised20081016.pdf 305263 B Adobe PDF
reviewfigures20081010.pdf 3300564 B Adobe PDF