Journal
PLOS ONE
Volume 6, Issue 12, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0028587
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Funding
- National Institutes of Health [AI061042, HL088203]
- National Science Foundation [MCB-0923661]
- Department of Defense [BC06911]
- Maryland Stem Cell Research Fund [MSCRFE-0043-00]
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [0923661] Funding Source: National Science Foundation
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Rac1 influences a multiplicity of vital cellular-and tissue-level control functions, making it an important candidate for targeted therapeutics. The activity of the Rho family member Cdc42 has been shown to be modulated by tyrosine phosphorylation at position 64. We therefore investigated consequences of the point mutations Y64F and Y64D in Rac1. Both mutations altered cell spreading from baseline in the settings of wild type, constitutively active, or dominant negative Rac1 expression, and were accompanied by differences in Rac1 targeting to focal adhesions. Rac1-Y64F displayed increased GTP-binding, increased association with beta PIX, and reduced binding with RhoGDI as compared with wild type Rac1. Rac1-Y64D had less binding to PAK than Rac1-WT or Rac1-64F. In vitro assays demonstrated that Y64 in Rac1 is a target for FAK and Src. Taken together, these data suggest a mechanism for the regulation of Rac1 activity by non-receptor tyrosine kinases, with consequences for membrane extension.
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