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Ras-related protein Rab-33B (RAB33B) is a small GTPase belonging to the Rab protein family, ubiquitously expressed in tissues. It orchestrates vesicle-mediated transport, primarily at the Golgi, regulating retrograde traffic from the Golgi to the endoplasmic reticulum and facilitating autophagosome formation by interacting with effectors such as Atg16L1. RAB33B plays a key role in Golgi homeostasis, endocytosis, and intracellular transport of proteins, and is crucial for cellular autophagy pathways. Mutations in RAB33B are causative for rare autosomal recessive skeletal dysplasia syndromes such as Smith-McCort and Dyggve-Melchior-Clausen. Recent research indicates that RAB33B is also exploited by influenza viruses to transport viral proteins to the plasma membrane through autophagy-based vesicles. No approved drugs target RAB33B directly, but its interaction with autophagy and vesicular machinery makes it a potential target for future therapeutic interventions, especially relevant in infections and possibly other trafficking-related disorders.
Modulation of autophagy (inhibition or activation alters RAB33B interactions and trafficking); Drugs affecting vesicle trafficking or Golgi function may indirectly influence RAB33B function
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