G-Protein Gα13 Functions with Abl Kinase to Regulate Actin Cytoskeletal Reorganization. Academic Article uri icon

Overview

abstract

  • Heterotrimeric G-proteins are essential cellular signal transducers. One of the G-proteins, Gα13, is critical for actin cytoskeletal reorganization, cell migration, cell proliferation, and apoptosis. Previously, we have shown that Gα13 is essential for both G-protein-coupled receptor and receptor tyrosine kinase-induced actin cytoskeletal reorganization such as dynamic dorsal ruffle turnover and cell migration. However, the mechanism by which Gα13 signals to actin cytoskeletal reorganization is not completely understood. Here we show that Gα13 directly interacts with Abl tyrosine kinase, which is a critical regulator of actin cytoskeleton. This interaction is critical for Gα13-induced dorsal ruffle turnover, endothelial cell remodeling, and cell migration. Our data uncover a new molecular signaling pathway by which Gα13 controls actin cytoskeletal reorganization.

publication date

  • October 25, 2017

Research

keywords

  • Actin Cytoskeleton
  • Cell Movement
  • Embryo, Mammalian
  • Fibroblasts
  • GTP-Binding Protein alpha Subunits, G12-G13
  • Oncogene Proteins v-abl

Identity

PubMed Central ID

  • PMC5705571

Scopus Document Identifier

  • 85032926412

Digital Object Identifier (DOI)

  • 10.1016/j.jmb.2017.10.020

PubMed ID

  • 29079481

Additional Document Info

volume

  • 429

issue

  • 24