ArticleCell death & disease2016
Golgi-associated LC3 lipidation requires V-ATPase in noncanonical autophagy.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 64 citations in OpenAlex.
- A role for CASM in the repair of damaged Golgi architecture.Autophagy · 2026Article
- The V-ATPase/ATG16L1 axis drives membrane remodeling during epithelial morphogenesis.Nature communications · 2026Article
- Tributyltin induces conjugation of ATG8s to single membranes via the V-ATPase-ATG16L1 axis, leading to transcription factor EB activation in human cell lines.Archives of toxicology · 2026Article
- Inactive ryanodine receptors sustain lysosomal availability for autophagy by promoting ER-lysosomal contact site formation.Nature communications · 2026Article
- STING: a multifaced player in cellular homeostasis.Human molecular genetics · 2025Review
- A role for CASM in the repair of damaged Golgi architecture.bioRxiv : the preprint server for biology · 2025Article
- ATG8ylation-mediated tonoplast invagination mitigates vacuole damage.Nature communications · 2025Article
- The Emerging Roles of Vacuolar-Type ATPase-Dependent Lysosomal Acidification in Cardiovascular Disease.Biomolecules · 2025Review
- Contactin -Associated protein1 Regulates Autophagy by Modulating the PI3K/AKT/mTOR Signaling Pathway and ATG4B Levels in Vitro and in Vivo.Molecular neurobiology · 2025Article
- RAB33A promotes metastasis via RhoC accumulation through non-canonical autophagy in cervical cancer.Cell death & disease · 2025Article
- Lysosome-associated CASM: from upstream triggers to downstream effector mechanisms.Frontiers in cell and developmental biology · 2025Review
- CARMIL1-AA selectively inhibits macropinocytosis while sparing autophagy.Molecular biology of the cell · 2025Article
- Mechanisms and roles of membrane-anchored ATG8s.Frontiers in cell and developmental biology · 2025Review
- Lysosomes' fallback strategies: more than just survival or death.Frontiers in cell and developmental biology · 2025Review
- Lack of WDFY4 leads to impaired immune response and poor cancer prognosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Non-autophagic Golgi-LC3 lipidation facilitates TFE3 stress response against Golgi dysfunction.The EMBO journal · 2024Article
- Targeting Lipid Metabolism in Cancer Stem Cells for Anticancer Treatment.International journal of molecular sciences · 2024Review
- Sigma-1 receptor recruits LC3 mRNA to ER-associated omegasomes to promote localized LC3 translation enabling functional autophagy.Cell reports · 2024Article
- Conjugation of ATG8s to single membranes at a glance.Journal of cell science · 2024Review
- Missing WD40 Repeats in ATG16L1 Delays Canonical Autophagy and Inhibits Noncanonical Autophagy.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Autophagy is an evolutionarily conserved catabolic process by which cells degrade intracellular proteins and organelles in the lysosomes. Canonical autophagy requires all autophagy proteins (ATGs), whereas noncanonical autophagy is activated by diverse agents in which some of the essential autophagy proteins are dispensable. How noncanonical autophagy is induced and/or inhibited is still largely unclear. In this study, we demonstrated that AMDE-1, a recently identified chemical that can induce canonical autophagy, was able to elicit noncanonical autophagy that is independent of the ULK1 (unc-51-like kinase 1) complex and the Beclin1 complex. AMDE-1-induced noncanonical autophagy could be specifically suppressed by various V-ATPase (vacuolar-type H(+)-ATPase) inhibitors, but not by disturbance of the lysosome function or the intracellular ion redistribution. Similar findings were applicable to a diverse group of stimuli that can induce noncanonical autophagy in a FIP200-independent manner. AMDE-1-induced LC3 lipidation was colocalized with the Golgi complex, and was inhibited by the disturbance of Golgi complex. The integrity of the Golgi complex was also required for multiple other agents to stimulate noncanonical LC3 lipidation. These results suggest that the Golgi complex may serve as a membrane platform for noncanonical autophagy where V-ATPase is a key player. V-ATPase inhibitors could be useful tools for studying noncanonical autophagy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.