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Autophagy-associated proteins collectively refer to the suite of genes and proteins (predominantly called ATG proteins) that control and implement the biological process of autophagy, which is a conserved lysosome-dependent degradation pathway involved in cellular clearance and quality control. These proteins assemble into multiprotein complexes to regulate the initiation (e.g., ULK1/2, ATG13, FIP200), nucleation (e.g., Beclin-1, VPS34), expansion (e.g., ATG5, ATG7, ATG12, LC3), and completion (e.g., SNAREs, ATG4) of autophagosomes, as well as cargo recognition and fusion with lysosomes. Autophagy proteins are essential for cellular response to nutrient deprivation, clearance of damaged organelles, protein aggregates, and pathogens, and are implicated in a wide range of physiological and pathological processes, including cancer, neurodegeneration, infection, and inflammation. The term refers to a protein family/mechanistic module, not a single pharmacological target.
Inhibition or activation of autophagy (e.g., mTOR inhibitors activate, lysosomal inhibitors block late steps) Modulation of autophagy initiation (ULK1/Beclin-1 targeting) Blockade of autophagosome-lysosome fusion Interference with autophagy-related signaling cascades
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