Human ATG2B knockout HeLa cell lysate

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

ATG2B also known as Autophagy-related protein 2 homolog B plays a significant role in the autophagy process. This protein encodes a part of the essential machinery for the expansion of the autophagosome which is important for cellular degradation and recycling of cytoplasmic components. ATG2B has a molecular mass of approximately 223 kDa and shows expression in various tissues with higher levels observed in the heart and liver. Scientists study ATG2B due to its important function in maintaining cellular homeostasis.

Biological function summary

The protein facilitates the transfer of lipids necessary for the elongation of the pre-autophagosomal structure. ATG2B acts as a critical component of the ATG protein complex interacting closely with ATG9A and WIPI1 proteins. Through this complex ATG2B supports the formation and growth of autophagic membranes playing a pivotal role in cellular stress responses. The protein also affects cargo recognition during autophagy thereby influencing the selectivity of molecules degraded within the lysosome.

Pathways

The autophagy process significantly involves ATG2B within its regulatory mechanisms. This protein interacts actively in the mechanistic target of rapamycin (mTOR) signaling pathway which controls autophagy initiation and progression based on cellular nutrient status. Furthermore ATG2B shares collaborations with other related proteins within the phosphatidylinositol 3-kinase (PI3K) pathway linking it to lipid signaling mediations. These associations reinforce its role in maintaining cell survival pathways by degradation of damaged organelles and proteins.

Scientists have linked ATG2B to conditions like cancer and neurodegenerative diseases. The malfunction or alteration of ATG2B functions may result in defective autophagy contributing to the growth and survival of cancer cells by disrupting normal cellular cleanup processes. Similarly impaired ATG2B-mediated autophagy can lead to the accumulation of dysfunctional proteins a hallmark of diseases like Parkinson's. Additionally there are associations between ATG2B and proteins such as alpha-synuclein in these neurodegenerative contexts indicating a potential role in the pathology of these disorders.