Regulator of G Protein Signaling 1 (RGS1) Markedly Impairs Giα Signaling Responses of B Lymphocytes
Author(s) -
Chantal Moratz,
Veronica H. Kang,
Kirk M. Druey,
Chong-Shan Shi,
Astrid Scheschonka,
Philip M. Murphy,
Tohru Kozasa,
John H. Kehrl
Publication year - 2000
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.164.4.1829
Subject(s) - regulator of g protein signaling , heterotrimeric g protein , microbiology and biotechnology , gtpase activating protein , g protein , signal transduction , regulator , biology , biochemistry , gene
Regulator of G protein signaling (RGS) proteins modulate signaling through pathways that use heterotrimeric G proteins as transducing elements. RGS1 is expressed at high levels in certain B cell lines and can be induced in normal B cells by treatment with TNF-alpha. To determine the signaling pathways that RGS1 may regulate, we examined the specificity of RGS1 for various G alpha subunits and assessed its effect on chemokine signaling. G protein binding and GTPase assays revealed that RGS1 is a Gi alpha and Gq alpha GTPase-activating protein and a potential G12 alpha effector antagonist. Functional studies demonstrated that RGS1 impairs platelet activating factor-mediated increases in intracellular Ca+2, stromal-derived factor-1-induced cell migration, and the induction of downstream signaling by a constitutively active form of G12 alpha. Furthermore, germinal center B lymphocytes, which are refractory to stromal-derived factor-1-triggered migration, express high levels of RGS1. These results indicate that RGS proteins can profoundly effect the directed migration of lymphoid cells.
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