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Kinesin family member 3B (KIF3B) is a microtubule-based **molecular motor protein** of the kinesin-2 subfamily, widely expressed in human tissues[1][8]. It forms a heterodimer with KIF3A and associates with KAP3 to create a heterotrimeric complex required for **anterograde transport** of vesicles, organelles, and protein complexes along microtubules, utilizing ATP hydrolysis for movement[1][5][6]. KIF3B is crucial for several key cellular processes including **chromosome movement during mitosis and meiosis**, establishment and maintenance of cilia (intracellular transport known as intraflagellar transport or IFT), regulation of neuronal dendritic architecture, and trafficking of membrane proteins such as the NMDA receptor subunit NR2A[3][9]. Mutations or dysregulation of KIF3B are implicated in **ciliopathies** (including certain forms of inherited retina degeneration), and its upregulation is associated with enhanced cell proliferation and poor outcomes in multiple types of solid tumors, establishing it as a candidate therapeutic target[7][8]. No approved small molecules or targeted drugs inhibit KIF3B directly, and its essential cellular role suggests systemic inhibition could pose significant safety challenges.
Not applicable; no direct targeting by approved drugs reported. Research use may include shRNA-mediated knockdown or genetic manipulation to impact cancer cell proliferation or neuronal morphology[2][7].
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