Plasma membrane-associated small GTPase which cycles between an active GTP-bound and inactive GDP-bound state. In active state binds to a variety of effector proteins to regulate cellular responses, such as cell spreading and the formation of actin-based protusions including lamellipodia and membrane ruffles. Promotes cell adhesion and spreading on fibrinogen in a CIB1 and alpha-IIb/beta3 integrin-mediated manner. GTP + H2O = GDP + H(+) + phosphate Regulated by guanine nucleotide exchange factors (GEFs) which promote the exchange of bound GDP for free GTP, GTPase activating proteins (GAPs) which increase the GTP hydrolysis activity, and GDP dissociation inhibitors which inhibit the dissociation of the nucleotide from the GTPase. Regulated by the GEF protein DOCK7. Interacts with the GEF protein DOCK7, which promotes the exchange between GDP and GTP, and therefore activates it (PubMed:16982419). Interacts with C1D (PubMed:9852280). Interacts (via C-terminal region) with CIB1; the interaction induces their association with the cytoskeleton upon alpha-IIb/beta3 integrin-mediated adhesion (PubMed:11756406). Interacts with NRBP (PubMed:11956649). Membrane-associated when activated. Colocalizes with NRBP to endomembranes and at the cell periphery in lamellipodia. Colocalized with CIB1 in the perinuclear area and at the cell periphery. Highest levels in brain, also detected in heart, placenta and pancreas. Expression down-regulated in quiescent fibroblasts and clearly induced by serum stimulation. (Microbial infection) Glycosylated at Tyr-32 by Photorhabdus asymbiotica toxin PAU_02230. Mono-O-GlcNAcylation by PAU_02230 inhibits downstream signaling by an impaired interaction with diverse regulator and effector proteins of Rac and leads to actin disassembly. The disease is caused by variants affecting the gene represented in this entry. Belongs to the small GTPase superfamily. Rho family.