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TBC1 domain family member 17 (TBC1D17) is a protein-coding gene encoding a probable Rab GTPase-activating protein that negatively regulates Rab8A/B-mediated endocytic trafficking, thereby modulating vesicle-mediated transport in cells[1]. TBC1D17 is involved in key cellular processes including retrograde transport from endosomes to the Golgi and the regulation of autophagy and mitophagy—the selective degradation of mitochondria—through its action as a Rab-GAP[1][2][8]. It helps maintain cellular logistics by regulating membrane fusion processes, and localizes predominantly to the cytosol[1]. Diseases associated with mutations or dysregulation of TBC1D17 include primary open-angle glaucoma and normal tension glaucoma, and its broader family has been implicated in cancer metabolism, especially in breast cancer[1][6]. No drugs directly targeting TBC1D17 are currently known, and it is not listed as a biomarker or safety liability at this time[1].
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