RGS1 is a GTPase activating protein (GAP) for Gαi and Gαq and a member of the R4 family of RGS proteins. Transient transfection assays have shown that RGS1 attenuates G protein-coupled receptor (GPCR)-mediated signaling pathways. Studies performed using Rgs1-deficient mouse immune cells, or cells with reduced expression of human RGS1, show the expected enhancement in GPCR signaling. By contrast, RGS1, along RGS3 and RGS4, is reported to dramatically accelerate the activation kinetics of Gβγ-activated inwardly rectifying K+ channels in reconstituted Xenopus oocytes. Human RGS1 was first identified as a novel gene by subtractive cDNA cloning of activated B cells against activated T lymphocytes, and was highly expressed in peripheral blood mononuclear cells from a patient with B-cell acute lymphocytic leukemia. RGS1 expression is modulated in a variety of patho-physiological conditions including cancer, innate immune response through Toll-like receptor activation, and infection. Rgs1-targeted mice show abnormal B-cell and dendritic cell responses to chemokines, abnormal immune tissue architecture and defective lymphocyte trafficking.
Alternative names for this molecule:
1R20; BL34; IER1; IR20; Regulator of G protein signaling 1; Rgs1