Involvement of protein tyrosine phosphatases in activation of the trimeric G protein Gq/11

Oncogene. 1999 Dec 2;18(51):7399-402. doi: 10.1038/sj.onc.1203152.

Abstract

A variety of receptors coupled to the heterotrimeric guanine nucleotide-binding protein Gq/11 stimulate intracellular Ca2+ release through inositol (1,4,5)-trisphosphate (IP3) formation. We previously reported that tyrosine phosphorylation of the alpha subunit of the Gq/11 protein by protein tyrosine kinases (PTKs) regulates the activation of Gq/11 protein. Here we show that protein tyrosine phosphatases (PTPs) are also essential for Gq/11 protein activation. We find that Gq/11 protein-coupled receptor-mediated formation of IP3 is blocked by PTP inhibitors as well as PTK inhibitors. These inhibitors act prior to Gq/11 protein activation. Tyrosine phosphorylation of the alpha subunit of Gq/11 appears to inhibit its interaction with receptors. Thus, PTP is required for controlling the level of tyrosine phosphorylation of the alpha subunit of Gq/11 to promote its interaction with receptors. Therefore, we conclude that PTKs and PTPs co-operate to proceed activation cycle of the Gq/11 protein through tyrosine phosphorylation and de-phosphorylation of the alpha subunit of Gq/11.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CHO Cells
  • Cricetinae
  • GTP-Binding Proteins / metabolism*
  • Phosphorylation
  • Protein Tyrosine Phosphatases / metabolism*
  • Signal Transduction*

Substances

  • Protein Tyrosine Phosphatases
  • GTP-Binding Proteins