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Cell. 2004 Jan 23;116(2 Suppl):S23-5, 2 p following S25.
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Cell. 2004 Jan 23;116(2):167-79.
The small GTP-binding protein rac regulates growth factor-induced membrane ruffling.
Institute for Cancer Research, Chester Beatty Laboratories, London, England.
The function of rac, a ras-related GTP-binding protein, was investigated in fibroblasts by microinjection. In confluent serum-starved Swiss 3T3 cells, rac1 rapidly stimulated actin filament accumulation at the plasma membrane, forming membrane ruffles. Several growth factors and activated H-ras also induced membrane ruffling, and this response was prevented by a dominant inhibitory mutant rac protein, N17rac1. This suggests that endogenous rac proteins are required for growth factor-induced membrane ruffling. In addition to membrane ruffling, a later response to both rac1 microinjection and some growth factors was the formation of actin stress fibers, a process requiring endogenous rho proteins. Using N17rac1 we have shown that these growth factors act through rac to stimulate this rho-dependent response. We propose that rac and rho are essential components of signal transduction pathways linking growth factors to the organization of polymerized actin.
PMID: 1643658 [PubMed - indexed for MEDLINE]