ArticleNature communications2019
Gigaxonin E3 ligase governs ATG16L1 turnover to control autophagosome production.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Disease mutation in gigaxonin-E3 ligase recapitulates giant axonal neuropathy in mice.Acta neuropathologica communications · 2025Article
- Gigaxonin Potentiates Antiviral Innate Immune Responses by Targeting cGAS and TREX1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SRAS1.1 E3 ligase mediates DSK2A degradation to regulate autophagy and drought tolerance in Arabidopsis.EMBO reports · 2025Article
- Mitochondrial damage triggers the concerted degradation of negative regulators of neuronal autophagy.Nature communications · 2025Article
- Article
- Pellino 3 E3 ligase promotes starvation-induced autophagy to prevent hepatic steatosis.Science advances · 2025Article
- ZDHHC7-mediatedAutophagy · 2024Article
- Ubiquitination regulates autophagy in cancer: simple modifications, promising targets.Journal of translational medicine · 2024Review
- Ubiquitin system mutations in neurological diseases.Trends in biochemical sciences · 2024Review
- Gigaxonin, mutated in Giant Axonal Neuropathy, interacts with TDP-43 and other RNA binding proteins.bioRxiv : the preprint server for biology · 2024Article
- Interlinked destinies: How ubiquitin-proteasome and autophagy systems underpin neurocognitive outcomes.Experimental neurology · 2024Review
- Gigaxonin Suppresses Epithelial-to-Mesenchymal Transition of Human Cancer Through Downregulation of Snail.Cancer research communications · 2024Article
- Review
- Lens autophagy protein ATG16L1: a potential target for cataract treatment.Theranostics · 2024Article
- A multilevel screening pipeline in zebrafish identifies therapeutic drugs for GAN.EMBO molecular medicine · 2023Article
- Article
- Autophagy/Mitophagy Regulated by Ubiquitination: A Promising Pathway in Cancer Therapeutics.Cancers · 2023Review
- To Kill or to Be Killed: How Does the Battle between the UPS and Autophagy Maintain the Intracellular Homeostasis in Eukaryotes?International journal of molecular sciences · 2023Review
- Advances in the potential roles of Cullin-RING ligases in regulating autoimmune diseases.Frontiers in immunology · 2023Review
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is an essential self-digestion machinery for cell survival and homoeostasis. Membrane elongation is fundamental, as it drives the formation of the double-membrane vesicles that engulf cytosolic material. LC3-lipidation, the signature of autophagosome formation, results from a complex ubiquitin-conjugating cascade orchestrated by the ATG16L1 protein, whose regulation is unknown. Here, we identify the Gigaxonin-E3 ligase as the first regulator of ATG16L1 turn-over and autophagosome production. Gigaxonin interacts with the WD40 domain of ATG16L1 to drive its ubiquitination and subsequent degradation. Gigaxonin depletion induces the formation of ATG16L1 aggregates and impairs LC3 lipidation, hence altering lysosomal fusion and degradation of the main autophagy receptor p62. Altogether, we demonstrate that the Gigaxonin-E3 ligase controls the production of autophagosomes by a reversible, ubiquitin-dependent process selective for ATG16L1. Our findings unveil the fundamental mechanisms of the control of autophagosome formation, and provide a molecular switch to fine-tune the activation of 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.