Rho GTPase-activating protein 22 (ARHGAP22)

Rho GTPase-activating protein 22 (ARHGAP22) is an enzyme of the Rho GTPase-activating protein family, responsible for turning off Rho GTPases, especially RAC1, by enhancing their intrinsic GTPase activity and converting them to the inactive GDP-bound state. ARHGAP22 is widely expressed, with high levels in vascular tissues and in the central nervous system. It regulates actin cytoskeletal dynamics, endothelial cell angiogenesis, cell motility, and synapse formation, and is essential in modulating neurodevelopmental processes such as dendritic spine density and synaptic plasticity, as well as vascular responses and wound repair. Dysregulation of ARHGAP22 is implicated in cancer cell migration (e.g., melanoma), diabetic retinopathy, cognitive disorders, and other complex pathologies. Epigenetic modifications and genetic variants in ARHGAP22 serve as potential biomarkers for disease susceptibility and progression[1][2][3].

Other names

RhoGAP2RhoGap22RHOGAP2Rho-type GTPase-activating protein 22rho GTPase-activating protein 22rho-type GTPase-activating protein 22

Inhibition of RAC1 activity via stimulation of GTPase activity (inactivating RAC1); for drugs like NSC23766, direct inhibition of RAC1 GEF activity