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Beclin 2 is a mammalian-specific member of the Beclin (BECN) family of autophagy regulators, encoded by the BECN2 gene. It participates in two mechanistically distinct lysosomal degradation pathways: canonical autophagy, and ligand-induced endolysosomal degradation of select G protein-coupled receptors (GPCRs) through interaction with the GPCR-associated sorting protein GASP1. In autophagy, Beclin 2 physically interacts with several proteins of the class III phosphoinositide 3-kinase (PI3K) complex and regulates the formation of autophagosomes. In endolysosomal trafficking, Beclin 2 controls the degradation of a subset of GPCRs, including δ-opioid and cannabinoid 1 receptors, a function not shared by its paralog Beclin 1. Genetic deletion of Beclin 2 in mice results in autophagy defects, altered GPCR turnover, increased food intake, obesity, and insulin resistance, highlighting a previously unrecognized link between autophagy, receptor sorting, and metabolic regulation[1][2][3].
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