Autophagy-related protein 2 homolog A (ATG2A)

Autophagy-related protein 2 homolog A (ATG2A) is a large, evolutionarily conserved protein essential for the process of macroautophagy, a pathway that mediates delivery of cytoplasmic materials to lysosomes for degradation[1][2][3]. ATG2A functions as a bridge-like lipid transfer protein, enabling transfer of lipids from the endoplasmic reticulum or endosomes to the expanding phagophore (precursor to the autophagosome)[3][4][5]. It forms complexes with WIPI proteins (notably WIPI4) and localizes to both isolation membranes/autophagosomes and lipid droplets[1][2]. Depletion of ATG2A (and its redundant paralog ATG2B) blocks autophagosome formation and autophagosome-mediated degradation, underscoring its essential role in autophagy and lipid homeostasis[2][4][5]. While not yet pursued directly as a therapeutic target, ATG2A’s critical role in autophagy links it to various conditions involving defective autophagic flux, such as cancer, neurodegeneration, and metabolic disorders[3][4]. No known drugs directly target ATG2A in clinical use, and ATG2A is not a standard biomarker for patient selection[2][3].

Other names

ATG2AKIAA0404BLTP4ABridge-like lipid transfer protein family member 4A