McCormick, 1993). The Rho-family members regulate a Stowers, 1995). The cyclical production of these actin-based ty. In

hich bers dates that ts on the inase whether Graf acted at the level of Cdc42, Rho, or both in Conversely, Graf expression does not inhibit bradykininvariety of cellular responses including actin polymerization and reorganization, gene expression (p38/JNK and SRF activity), cleavage furrow formation, G1 cell cycle progression, endocytosis, exocytosis, and superoxide production (Ridley, 1996). Cytoskeletal rearrangement is one of the best characterized responses of Rho-family members. Studies employing quiescent Swiss 3T3 cells have indicated that Rho-dependent regulation of the cytoskeleton involves signaling through Cdc42, Rac and Rho (Hall, 1998). In these cells activation of Cdc42 (by bradykinin, tumor necrosis factor- a (TNF- a) and IL-1 (interleukin-1)) stimulates the formation of finger-like projections of actin filaments called filopodia. Activation of structures is proposed to be important for cellular motili fact, activated Cdc42 and Rac increase the motility invasiveness of mammary carcinoma cells (Keely et al., 1 and a dominant-interfering mutant for Rac blocks PD stimulated migration of Rat-1 fibroblasts (Anand-Apte e 1997). The downstream effectors of Cdc42, Rac and Rho w lead to the assembly of filopodia, lamellipodia and stress fi are not fully understood; however, some potential candi have been recently identified. Some evidence suggests smw G proteins utilize protein kinases to elicit their effec actin polymerization. Both Cdc42 and Rac activate tyrosine kinase Ack as well as the serine/threonine kINTRODUCTION The small molecular weight GTP-binding proteins (smw