Autophagy-related protein 2 homolog B (ATG2B)

Autophagy-related protein 2 homolog B (ATG2B) is a large, evolutionarily conserved protein crucial for autophagy, particularly for the formation of autophagosomes, which are double-membrane vesicles responsible for the delivery of cytoplasmic material to lysosomes for degradation[1][3][4]. ATG2B functions as a lipid transfer protein that tethers the edge of the isolation membrane (phagophore) to the endoplasmic reticulum and mediates direct phospholipid transport from the endoplasmic reticulum, facilitating membrane expansion required for autophagosome biogenesis[1][2]. The activity of ATG2B is regulated by interaction with other autophagy proteins, including Atg18 orthologs (e.g., WIPI4) and negatively charged membranes[2]. Disruption of ATG2B impairs autophagosome closure, leads to accumulation of autophagic structures, and affects the size and distribution of lipid droplets independently of autophagy[3][4]. Germline ATG2B alterations are linked to increased risk of myeloid malignancies and are associated with neurodegenerative disease[1]. So far, no drugs directly targeting ATG2B are reported, nor is it established as a routine biomarker or safety concern in clinical therapy.

Other names

ATG2BC14orf103FLJ10242BLTP4Bbridge-like lipid transfer protein family member 4BATG2 autophagy related 2 homolog B