The G protein G alpha(13) is required for growth factor-induced cell migration. Academic Article uri icon

Overview

abstract

  • Heterotrimeric G proteins are critical cellular signal transducers. They are known to directly relay signals from seven-transmembrane G protein-coupled receptors (GPCRs) to downstream effectors. On the other hand, receptor tyrosine kinases (RTKs), a different family of membrane receptors, signal through docking sites in their carboxy-terminal tails created by autophosphorylated tyrosine residues. Here we show that a heterotrimeric G protein, G alpha(13), is essential for RTK-induced migration of mouse fibroblast and endothelial cells. G alpha(13) activity in cell migration is retained in a C-terminal mutant that is defective in GPCR coupling, suggesting that the migration function is independent of GPCR signaling. Thus, G alpha(13) appears to be a critical signal transducer for RTKs as well as GPCRs. This broader role of G alpha(13) in cell migration initiated by two types of receptors could provide a molecular basis for the vascular system defects exhibited by G alpha(13) knockout mice.

publication date

  • June 1, 2006

Research

keywords

  • Cell Movement
  • Epidermal Growth Factor
  • GTP-Binding Protein alpha Subunits, G12-G13
  • Platelet-Derived Growth Factor
  • Receptor Protein-Tyrosine Kinases

Identity

Scopus Document Identifier

  • 33646859037

Digital Object Identifier (DOI)

  • 10.1016/j.devcel.2006.03.014

PubMed ID

  • 16740474

Additional Document Info

volume

  • 10

issue

  • 6