Control of cell polarity and chemotaxis by Akt/PKB and PI3 kinase through the regulation of PAKa.

Published

Journal Article

We demonstrate that PI3 kinase and protein kinase B (PKB or Akt) control cell polarity and chemotaxis, in part, through the regulation of PAKa, which is required for myosin II assembly. We demonstrate that PI3K and PKB mediate PAKa's subcellular localization, PAKa's activation in response to chemoattractant stimulation, and chemoattractant-mediated myosin II assembly. Mutation of the PKB phosphorylation site in PAKa to Ala blocks PAKa's activation and inhibits PAKa redistribution in response to chemoattractant stimulation, whereas an Asp substitution leads to an activated protein. Addition of the PI3K inhibitor LY294002 results in a rapid loss of cell polarity and the axial distribution of actin, myosin, and PAKa. These results provide a mechanism by which PI3K regulates chemotaxis.

Full Text

Duke Authors

Cited Authors

  • Chung, CY; Potikyan, G; Firtel, RA

Published Date

  • May 2001

Published In

Volume / Issue

  • 7 / 5

Start / End Page

  • 937 - 947

PubMed ID

  • 11389841

Pubmed Central ID

  • 11389841

Electronic International Standard Serial Number (EISSN)

  • 1097-4164

International Standard Serial Number (ISSN)

  • 1097-2765

Digital Object Identifier (DOI)

  • 10.1016/s1097-2765(01)00247-7

Language

  • eng