ATG4B

From WikiMD's Food, Medicine & Wellness Encyclopedia

Protein ATG4B PDB 2cy7

ATG4B

ATG4B is a gene that encodes a protein involved in the process of autophagy. Autophagy is a cellular mechanism responsible for degrading and recycling damaged or unnecessary components within the cell. The ATG4B protein plays a crucial role in the initiation of autophagy by cleaving a key protein called LC3, which is essential for the formation of autophagosomes.

Function[edit | edit source]

The primary function of ATG4B is to process LC3, a protein that is essential for the formation of autophagosomes. Autophagosomes are double-membrane vesicles that sequester cellular components targeted for degradation. By cleaving LC3, ATG4B facilitates the lipidation of LC3, which is necessary for its association with the autophagosomal membrane.

Regulation[edit | edit source]

ATG4B activity is tightly regulated to ensure proper autophagy function. Post-translational modifications, such as phosphorylation, can modulate the activity of ATG4B and its interaction with LC3. Additionally, ATG4B expression levels can be influenced by various cellular stress conditions, such as nutrient deprivation or oxidative stress, which are known to induce autophagy.

Clinical Implications[edit | edit source]

Dysregulation of autophagy, including aberrant ATG4B activity, has been implicated in various human diseases, including cancer, neurodegenerative disorders, and metabolic conditions. Targeting ATG4B and other components of the autophagy pathway has emerged as a potential therapeutic strategy for treating these diseases.

See Also[edit | edit source]

Wiki.png

Navigation: Wellness - Encyclopedia - Health topics - Disease Index‏‎ - Drugs - World Directory - Gray's Anatomy - Keto diet - Recipes

Search WikiMD


Ad.Tired of being Overweight? Try W8MD's physician weight loss program.
Semaglutide (Ozempic / Wegovy and Tirzepatide (Mounjaro / Zepbound) available.
Advertise on WikiMD

WikiMD is not a substitute for professional medical advice. See full disclaimer.

Credits:Most images are courtesy of Wikimedia commons, and templates Wikipedia, licensed under CC BY SA or similar.

Contributors: Prab R. Tumpati, MD