Interferon[beta]-1b Induces the Expression of RGS1 a Negative Regulator of G-Protein Signaling

We present evidence of a link between interferonβ-1b (IFN-β) and G-protein signaling by demonstrating that IFN-β can induce the expression of the negative regulator of G-protein signaling 1 (RGS1). RGS1 reduces G-protein activation and immune cell migration by interacting with heterotrimeric G-prote...

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Bibliographic Details
Published inInternational journal of cell biology Vol. 2010
Main Authors Tran, Tiffany, Paz, Pedro, Velichko, Sharlene, Cifrese, Jill, Belur, Praveen, Yamaguchi, Ken D, Ku, Karin, Parham Mirshahpanah, Reder, Anthony T, Croze, Ed
Format Journal Article
LanguageEnglish
Published New York Hindawi Limited 01.01.2010
Subjects
Apoptosis
Autoimmune diseases
Cell adhesion & migration
Immune system
Inflammatory bowel disease
Proteins
Regulation
Rheumatoid arthritis
Studies
Viral infections
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Summary:We present evidence of a link between interferonβ-1b (IFN-β) and G-protein signaling by demonstrating that IFN-β can induce the expression of the negative regulator of G-protein signaling 1 (RGS1). RGS1 reduces G-protein activation and immune cell migration by interacting with heterotrimeric G-proteins and enhancing their intrinsic GTPase activity. In this study, IFN-β treatment resulted in the induction of RGS1 in peripheral blood mononuclear cells (PBMCs), monocytes, T cells, and B cells. Induction of RGS1 by IFN-β was concentration dependent and observed at both the RNA and protein level. Other members of the RGS family were not induced by IFN-β, and induction of RGS1 required the activation of the IFN receptor. In addition, RGS1 induction was observed in PBMCs obtained from IFN-β-treated multiple sclerosis patients suggesting a possible, as yet unexplored, involvement of G-protein regulation in disease treatment. The upregulation of RGS1 by IFN-β has not been previously reported.
ISSN:1687-8876
1687-8884