Inquiry Basket
Loading ......
Filter By Product Search for
ATG16L1
ATG16L1 Full Name
autophagy related 16-like 1 (S. cerevisiae)
ATG16L1 Introduction
ATG16L1 (autophagy related 16-like 1) is a core autophagy-related protein that plays an essential role in the formation and maturation of autophagosomes, the double-membrane vesicles responsible for degrading damaged organelles, aggregated proteins, and intracellular pathogens. As the mammalian homolog of yeast Atg16, ATG16L1 is a key component of the ATG12–ATG5–ATG16L1 complex, which functions as an E3-like enzyme platform to promote LC3/ATG8 lipidation, a critical step required for autophagosome membrane expansion. Structurally, ATG16L1 contains an N-terminal ATG5-binding region, a coiled-coil domain involved in complex assembly, and a C-terminal WD40 domain that mediates interactions with membranes and regulatory proteins. Increasing evidence indicates that ATG16L1 is not simply an autophagy scaffold but a multifunctional regulator involved in membrane dynamics, intracellular trafficking, immune regulation, and maintenance of cellular homeostasis. Dysregulation of ATG16L1 activity can disrupt autophagic flux and cellular quality control mechanisms, making it an important research target for understanding diseases associated with defective protein clearance and abnormal inflammation.
Beyond its canonical role in autophagy, ATG16L1 contributes to multiple cellular processes that influence immune responses and tissue function. By controlling LC3 lipidation and autophagosome biogenesis, ATG16L1 regulates selective autophagy pathways such as xenophagy, which enables cells to eliminate invading microorganisms. ATG16L1 also participates in autophagy-independent mechanisms, including regulation of inflammatory signaling, vesicle transport, and epithelial cell homeostasis. One of the most studied examples is its role in intestinal immunity, where ATG16L1 variants, particularly the T300A polymorphism (rs2241880), have been strongly associated with increased susceptibility to Crohn's disease. This variant alters ATG16L1 stability and cellular responses to stress, affecting bacterial handling, inflammasome activation, and intestinal barrier integrity. These findings have highlighted ATG16L1 as a molecular link between autophagy dysfunction, innate immunity, and chronic inflammatory disorders.
ATG16L1 has emerged as a potential therapeutic target in research areas including inflammatory diseases, cardiovascular disorders, cancer, and infection biology. Abnormal ATG16L1 regulation has been implicated in impaired cellular stress adaptation, excessive inflammation, and altered immune surveillance. Genetic studies have also suggested that changes in the ATG16L1 promoter region may influence transcriptional activity and autophagy levels, potentially contributing to conditions such as acute myocardial infarction through altered cellular responses to injury. In oncology research, ATG16L1-mediated autophagy regulation is being investigated because tumor cells often exploit autophagy pathways to survive metabolic stress and therapeutic challenges. Understanding how ATG16L1 controls autophagic and non-autophagic functions provides valuable insights for developing targeted strategies to modulate immune activity, restore cellular homeostasis, and improve treatments for diseases driven by autophagy imbalance.
Alternate Names for ATG16L1
ATG16L1; autophagy related 16-like 1 (S. cerevisiae); IBD10; WDR30; APG16L; ATG16A; ATG16L; autophagy-related protein 16-1; APG16L beta; WD repeat domain 30; ATG16 autophagy related 16-like 1;
Loading ......
