Rho GTPase activating protein 26 (ARHGAP26)

Rho GTPase activating protein 26 (ARHGAP26) is an enzyme that inactivates Rho GTPases, particularly RhoA and Cdc42, by enhancing their intrinsic GTP hydrolysis, thereby negatively regulating Rho family signaling[1][4]. This protein plays a central role in actin cytoskeleton dynamics, cell migration, cell spreading, endocytosis, and maintenance of cell polarity. ARHGAP26 is recruited to sites of integrin signaling through interaction with focal adhesion kinase (FAK), linking extracellular signals to the internal organization of the cytoskeleton[1][2][4]. Abnormalities in ARHGAP26 expression or function—via gene fusion, altered methylation, or abnormal RNA splicing—are associated with various cancers, including a distinctive fusion with claudin-18 (CLDN18-ARHGAP26) in a subset of gastric cancers. In addition, ARHGAP26 or its derivatives may serve as disease biomarkers and are under consideration as possible therapeutic targets, particularly in cancers characterized by either overexpression, underexpression, or oncogenic gene fusion forms[2][3][4].

Other names

GRAFGRAF1KIAA0621OPHN1LOPHN1L1GTPase regulator associated with focal adhesion kinaseOligophrenin-1-like protein

Small molecules or biologics targeting ARHGAP26 would likely modulate its GAP activity, thus altering RhoA and Cdc42 activity and downstream signaling. - In cancer, therapeutic strategies might involve interfering with ARHGAP26 gene fusion products (such as CLDN18-ARHGAP26 in gastric cancer) or modulating its expression or degradation.[2]