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Ras-related C3 botulinum toxin substrate 3 (RAC3) is a plasma membrane-associated small GTPase that functions as a molecular switch by cycling between active GTP-bound and inactive GDP-bound states. It regulates processes such as actin cytoskeleton organization, cell adhesion, migration, signal transduction, vesicle trafficking, and neuronal development. RAC3 expression is more limited compared to other Rac isoforms, with higher levels in developing neurons and certain tumors. Pathogenic variants and abnormal gene expression are associated with neurodevelopmental disorders (intellectual disability, abnormal brain morphology) and several cancer types due to its critical roles in cell growth, motility, invasion, and metastasis. Knockdown or dysfunction of RAC3 leads to brain structure anomalies and can drive cancer progression through modulation of cell signaling pathways[1][2][3][4][5][6][7][8][9][10][11].
Drugs that inhibit GTPase activity (small molecule inhibitors targeting Rac signaling); Inhibition of effector pathways (e.g., PI3K, PAK1); Modulation of cell motility and invasion (via disruption of actin dynamics)
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