Aliases for RAC2 Gene
External Ids for RAC2 Gene
This gene encodes a member of the Ras superfamily of small guanosine triphosphate (GTP)-metabolizing proteins. The encoded protein localizes to the plasma membrane, where it regulates diverse processes, such as secretion, phagocytosis, and cell polarization. Activity of this protein is also involved in the generation of reactive oxygen species. Mutations in this gene are associated with neutrophil immunodeficiency syndrome. There is a pseudogene for this gene on chromosome 6. [provided by RefSeq, Jul 2013]
GeneCards Summary for RAC2 Gene
RAC2 (Ras-Related C3 Botulinum Toxin Substrate 2 (Rho Family, Small GTP Binding Protein Rac2)) is a Protein Coding gene. Diseases associated with RAC2 include neutrophil immunodeficiency syndrome. 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 RHOH.
UniProtKB/Swiss-Prot for RAC2 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 secretory processes, phagocytose of apoptotic cells and epithelial cell polarization. Augments the production of reactive oxygen species (ROS) by NADPH oxidase.
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.