Title : G-protein-coupled receptor (GPCR) kinase phosphorylation and beta-arrestin recruitment regulate the constitutive signaling activity of the human cytomegalovirus US28 GPCR.

Pub. Date : 2003 Jun 13

PMID : 12668664






3 Functional Relationships(s)
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1 Deletion of the carboxyl terminal 40 amino acids in US28 generates a receptor that is severely impaired in its ability to become phosphorylated and recruit beta-arrestin and accordingly demonstrates increased inositol phosphate signaling. Inositol Phosphates envelope protein US28 Human betaherpesvirus 5
2 In addition, overexpression of wild type GRK5 leads to hyperphosphorylation of US28 that results in a decrease of inositol phosphate accumulation. Inositol Phosphates envelope protein US28 Human betaherpesvirus 5
3 These results are consistent with the hypothesis that GRK phosphorylation and recruitment of beta-arrestin to the US28 viral GPCR attenuates signaling to the traditional Galphaq-stimulated inositol phosphate pathway. Inositol Phosphates envelope protein US28 Human betaherpesvirus 5