Aliases for ARHGDIA Gene
External Ids for ARHGDIA Gene
Previous HGNC Symbols for ARHGDIA Gene
Previous GeneCards Identifiers for ARHGDIA Gene
This gene encodes a protein that plays a key role in the regulation of signaling through Rho GTPases. The encoded protein inhibits the disassociation of Rho family members from GDP (guanine diphosphate), thereby maintaining these factors in an inactive state. Activity of this protein is important in a variety of cellular processes, and expression of this gene may be altered in tumors. Mutations in this gene have been found in individuals with nephrotic syndrome, type 8. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Jul 2014]
GeneCards Summary for ARHGDIA Gene
ARHGDIA (Rho GDP Dissociation Inhibitor Alpha) is a Protein Coding gene. Diseases associated with ARHGDIA include Nephrotic Syndrome, Type 8 and Familial Idiopathic Steroid-Resistant Nephrotic Syndrome With Diffuse Mesangial Sclerosis. Among its related pathways are G-protein signaling_Regulation of CDC42 activity and Vasopressin-regulated water reabsorption. GO annotations related to this gene include GTPase activator activity and Rho GDP-dissociation inhibitor activity. An important paralog of this gene is ARHGDIB.
UniProtKB/Swiss-Prot for ARHGDIA Gene
Controls Rho proteins homeostasis. Regulates the GDP/GTP exchange reaction of the Rho proteins by inhibiting the dissociation of GDP from them, and the subsequent binding of GTP to them. Retains Rho proteins such as CDC42, RAC1 and RHOA in an inactive cytosolic pool, regulating their stability and protecting them from degradation. Actively involved in the recycling and distribution of activated Rho GTPases in the cell, mediates extraction from membranes of both inactive and activated molecules due its exceptionally high affinity for prenylated forms. Through the modulation of Rho proteins, may play a role in cell motility regulation. In glioma cells, inhibits cell migration and invasion by mediating the signals of SEMA5A and PLXNB3 that lead to inactivation of RAC1.