Ras-related protein Rab-17 (Rab17)

Ras-related protein Rab-17 (Rab17) is a member of the Rab subfamily, part of the Ras small GTPase superfamily[1][4]. It acts as a key regulator of intracellular membrane trafficking, operating through cycles of GDP- and GTP-binding which control recruitment of downstream effectors for vesicle formation, movement, tethering, and fusion. Rab17 is particularly important in epithelial cells, where it mediates transcytosis and apical recycling endosome trafficking, essential for processes like immunoglobulin transport across epithelial barriers and melanosome release from melanocytes[1][4][5]. In neurons, Rab17 regulates dendrite and dendritic spine development, with knockdown leading to reduced dendritic growth and impaired filopodia formation[2]. Rab17 also plays significant roles in the immune system, directing membrane supply for antibacterial autophagy and affecting efferocytosis by regulating immune compartment trafficking[1]. In disease contexts, Rab17 acts as a tumor suppressor in hepatocellular carcinoma and non–small cell lung cancer models by reducing cell proliferation and migration; however, in endometrial cancer, elevated Rab17 inhibits ferroptosis and supports survival under hypoglycemia[1]. Mutations or altered expression of Rab17 are associated with Griscelli syndrome, Type 3, and Carpenter syndrome 1[4]. Direct drug targeting, biomarker use, or clinical safety concerns for Rab17 are not currently reported.

Other names

RAB17Ras-related protein Rab-17RAB17, member RAS oncogene familyras-related protein Rab-17

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