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• W2032102284 endingPage "2165" @default.
• W2032102284 startingPage "2155" @default.
• W2032102284 abstract "The G-protein α subunit, α13, regulates cell growth and differentiation through the monomeric Rho GTPase. α13 activates Rho through direct stimulation of the guanine nucleotide exchange factor p115RhoGEF, which contains a regulator of G-protein signaling homology domain (RH) in its N-terminus. Through its RH domain, p115RhoGEF also functions as a GAP for Gα13. The mechanism for the Gα13/p115RhoGEF interaction is not well understood. Here, we determined specific α13 residues important for its interaction with p115RhoGEF. GST-pulldowns and co-immunoprecipitation assays revealed that individually mutating α13 residues Lys204, Glu229, or Arg232 to opposite charge residues disrupts the interaction of activated α13 with the RH domain of p115RhoGEF or full-length p115RhoGEF. We further demonstrate that mutation of Glu229, and to a lesser extent Lys204 or Arg232, disrupts the ability of activated α13 to induce the recruitment of p115RhoGEF to the plasma membrane (PM) and to activate Rho-mediated serum response element-luciferase gene transcription. Interestingly, an α13 mutant where a conserved Gly was mutated to a Ser (G205S) retained its ability to bind to p115RhoGEF, induce p115RhoGEF recruitment to the PM, and activate Rho-dependent signaling, even though identical Gly to Ser mutations in other α disrupt their interaction with regulator of G-protein signaling (RGS) proteins. These results demonstrate that, whereas several features of a typical α/RGS interaction are preserved in the α13/p115RhoGEF interaction, there are also significant differences." @default.
• W2032102284 created "2016-06-24" @default.
• W2032102284 creator A5006519502 @default.
• W2032102284 creator A5030298250 @default.
• W2032102284 date "2005-02-14" @default.
• W2032102284 modified "2023-10-18" @default.
• W2032102284 title "Functional consequences of Gα13 mutations that disrupt interaction with p115RhoGEF" @default.
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• W2032102284 doi "https://doi.org/10.1038/sj.onc.1208414" @default.
• W2032102284 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1351220" @default.
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• W2032102284 hasPublicationYear "2005" @default.
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