9/5/2023 0 Comments Autophagy flaticonAutophagy also controls stem cell fate and defective autophagy is involved in many pathophysiological processes. This conserved process is essential for metabolic plasticity and tissue homeostasis and is crucial for mammalian post-mitotic cells. ULK1: Unc-51-like autophagy activating kinase 1, mTORC1: mammalian target of rapamycin complex 1, PI3K: Class III phosphatidylinositol 3-kinase, VPS34: phosphatidylinositol 3-kinase, PI3P: phosphatidylinositol-3-phosphate, WIPI: WD-repeat protein interacting with phosphoInositides, Atg: Autophagy-related gene, LC3: Microtubule-associated protein light chain 3, PE: Phosphatidylethanolamine, SNAP: Synaptosomal-associated protein, VAMP: Vesicle-associated membrane protein, SNARE: Soluble N-ethyl maleimide-sensitive protein (NSF) attachment protein receptor, STX: Syntaxin. Autophagy is a constitutive pathway that allows the lysosomal degradation of damaged components. Autophagosomes form SNAP29, and lysosome VAMP7/VAMP8 and SNARE conjugates by STX17 and YKT6 complexes, resulting in the fusion of autophagosomes and lysosomes. Autophagosome formation is completed by the LC3-PE complex and Atg12-Atg5-Atg16L1 complex. The Atg12-Atg5-Atg16L1 complex has E3-like activity against the LC3-PE complex on phagophores. VPS34 of the PI3K complex forms PI3P, and WIPI is mobilized, and WIPI2 acts on Atg2. The class III phosphatidylinositol 3-kinase (PtdIns3K) complex is mobilized downstream of the PI3K complex to form a phagophore. Amino acid starvation and reduced insulin levels lead to the inactivation of mTORC1, resulting in the induction of autophagy. ULK1 complex involved in initiating autophagy is regulated by mTORC1. All icons 1,640 Powerpoint Icons Display your business presentations with clear representation by applying PowerPoint icons in your cloud folder for your clients to see. This article provides a comprehensive review of the role of autophagy in health, physiological function, and autophagy-related disease.Īutophagy autophagy-related gene cancer cardiovascular liver disease mitophagy neurodegenerative disease. In addition to the discovery of certain disease-causing autophagy-related mutations and elucidation of the pathogenesis of conditions resulting from the abnormal degradation of selective autophagy substrates, the activation of autophagy is essential for prolonging life and suppressing aging. Recent studies have revealed that autophagy dysfunction is implicated in neurodegenerative diseases and tumorigenesis. In vivo, autophagy has been shown to be involved in the starvation response, intracellular quality control, early development, and cell differentiation. Autophagy plays an important role in maintaining and regulating cell homeostasis by degrading intracellular components and providing degradation products to cells. During fusion with the lysosome (blue oval) LC3–PE associated with the outer membrane is cleaved and recycled by ATG4 while LC3–PE associated with the inner-membrane is degraded by lysosomal proteases along with the cargo of the autophagosome.Autophagy refers to the process involving the decomposition of intracellular components via lysosomes. The membrane elongation is dependent on the ATG12–ATG5-ATG16L1 conjugation system. In the liver, autophagy participates in the basal turnover of lipids by engulfing and degrading lipid droplets ( 3 ). ( D) The autophagosomal membrane (orange crescent) is studded with LC3–PE (stylized in black). Autophagy is an adaptive, catabolic process that generates energy for cells under nutrient-starvation conditions and helps maintain cellular homeostasis in nutrient-rich environments through its constitutive activity ( 2 ). ( C) The two ubiquitin-like conjugation systems essential for membrane elongation are outlined schematically. BECN1 is inhibited when bound by anti-apoptotic BCL2, which results in downregulated autophagy. UVRAG and ATG14 are found in BECN1 complexes in a mutually exclusive manner. ( B) The PtdIns3K complex is assembled at the site of the nascent autophagosomal membrane. ( A) Dephosphorylated ULK1 dissociates from the MTOR complex and phosphorylates itself, ATG13 and RB1CC1 to induce the nucleation phase. ![]() Autophagy is a complex degradation process in which general cytoplasm or organelles are engulfed by a double-membrane bound structure and degraded and recycled following fusion with a lysosome.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |