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Vacuolar fusion protein MON1 homolog B (MON1B) is a cytoplasmic protein involved in multiple steps of intracellular vesicular trafficking, including transport from the endoplasmic reticulum (ER) to the Golgi apparatus and from the Golgi to the plasma membrane[1]. It operates as part of the Mon1-Ccz1 complex, which is essential for endocytic sorting and homotypic fusion of early endosomes, largely by recruiting to EEA1-positive vesicles in conjunction with the docking regulator Numb[3][4][5]. MON1B interacts with cytoplasmic dynein, modulating microtubule-dependent transport of vesicles, and may also influence Golgi apparatus morphology and secretory pathway efficiency[1]. It has a regulatory role in early and late viral transcription, especially during HSV-1 infection through down-regulation of promoter activation[2][5]. Mutations in MON1B have been linked to Joubert syndrome 31 and Brugada syndrome 9, indicating its necessity in proper vesicular traffic for physiological processes[5].
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