MON2 regulator of endosome-to-Golgi trafficking (MON2)

MON2 regulator of endosome-to-Golgi trafficking (MON2) is a conserved scaffold protein essential for proper vesicular transport between endosomes and the Golgi apparatus. MON2 localizes primarily to the trans-Golgi network and recycling endosomes[1][2]. Depletion of MON2 in mammalian cells accelerates the retrograde trafficking of transmembrane proteins such as furin and cation-independent mannose 6-phosphate receptor, suggesting it suppresses endosome-to-Golgi delivery under normal conditions[1]. In yeast, MON2 regulates retrograde transport, endocytosis, and vacuole biogenesis, interacting with proteins such as Dop1, Neo1, and GGA1. MON2 is required for the upregulation of autophagy, particularly under cellular stress (e.g., starvation), enhancing autophagosome formation via interaction with GABARAPL2[2][3]. Its role is implicated in the regulation of longevity in organisms, including *C. elegans*, by mediating trafficking and proper localization of autophagy factors, but no drugs, clinical biomarkers, or direct disease roles are currently established for MON2 in human medicine[2][3][4].

Other names

Protein MON2 homologKIAA1040SF21MON2 homologregulator of endosome-to-Golgi traffickingprotein SF21