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Rho GTPase activating protein 29 (ARHGAP29) is an enzyme that functions as a GTPase-activating protein (GAP) for members of the Rho-family of small GTPases, particularly RhoA, and to a lesser extent, Rac1 and CDC42[1][3]. By accelerating the hydrolysis of GTP, it inactivates these GTPases, regulating actin cytoskeleton assembly, cell shape, migration, proliferation, and invasion[3][2]. It is essential for processes such as endothelial cell function in vascular tubulogenesis and craniofacial development[1]. Genetic defects in ARHGAP29 are linked to nonsyndromic cleft lip/palate, and altered expression is implicated in the prognosis of several cancers, influencing tumor cell motility and invasiveness[1][2]. No approved drugs directly target ARHGAP29, but it is under active investigation as a mechanistic contributor and potential biomarker in oncology and developmental biology[2][3].
No drugs directly target ARHGAP29; however, suppression or modulation of its activity can impact RhoA signaling and cytoskeletal dynamics[2].
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