Aliases for RAC3 Gene
External Ids for RAC3 Gene
The protein encoded by this gene is a GTPase which belongs to the RAS superfamily of small GTP-binding proteins. Members of this superfamily appear to regulate a diverse array of cellular events, including the control of cell growth, cytoskeletal reorganization, and the activation of protein kinases. [provided by RefSeq, Jul 2008]
GeneCards Summary for RAC3 Gene
RAC3 (Ras-Related C3 Botulinum Toxin Substrate 3 (Rho Family, Small GTP Binding Protein Rac3)) is a Protein Coding gene. Among its related pathways are MAPK signaling pathway and Ras signaling pathway. GO annotations related to this gene include GTP binding and GTPase activity. An important paralog of this gene is RAC2.
UniProtKB/Swiss-Prot for RAC3 Gene
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.
Small G proteins (small GTPases) are homologous to Galpha proteins and are often referred to as the Ras proto-oncogene superfamily. The Ras superfamily contains over 100 small GTPases grouped into eight families; Ras, Rho, Rab, Rap, Arf, Ran, Rheb and Rad. Small GTPases regulate a wide variety of processes in the cell, including growth, differentiation, movement and lipid vesicle transport. Like Galpha proteins, small GTPases alternate between an on state (bound to GTP) and an off state (bound to GDP). This cyclic process requires guanine nucleotide exchange factor (GEF) and GTPase-activating protein (GAP). Small GTPases are the downstream effectors of most receptor tyrosine kinases (RTKs) and are linked via two proteins, GRB2 and SOS. They are coupled to intracellular signaling cascades including the MAPK pathway, through interactions with Raf kinase. Normally, activation of small GTPases is induced by ligand binding to a RTK. In many transformed cells activating mutations of GTPases, often Ras, produce a cellular response in the absence of a ligand, thus promoting malignant progression.