ArticleCommunications biology2021
Insights on autophagosome-lysosome tethering from structural and biochemical characterization of human autophagy factor EPG5.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Cutting edge: ESCRT-mediated phagophore closure in mammals.The Biochemical journal · 2026Review
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- Spatio-temporal processes in autophagosome-lysosome fusion.Medical review (2021) · 2025Review
- Structure of the human autophagy factor EPG5 and the molecular basis of its conserved mode of interaction with Atg8-family proteins.Autophagy · 2025Article
- Non-hormone replacement therapy to overcome premature ovarian insufficiency: advances in natural products and stem cells targeting autophagy.Frontiers in endocrinology · 2025Review
- A new perspective on the autophagic and non-autophagic functions of the GABARAP protein family: a potential therapeutic target for human diseases.Molecular and cellular biochemistry · 2024Review
- Review
- DYNATE: Localizing rare-variant association regions via multiple testing embedded in an aggregation tree.Genetic epidemiology · 2024Article
- Molecular structures and function of the autophagosome-lysosome fusion machinery.Autophagy reports · 2024Article
- Specific microRNAs for Modulation of Autophagy in Spinal Cord Injury.Brain sciences · 2022Review
- Review
- Vici syndrome in Israel: Clinical and molecular insights.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Pivotal to the maintenance of cellular homeostasis, macroautophagy (hereafter autophagy) is an evolutionarily conserved degradation system that involves sequestration of cytoplasmic material into the double-membrane autophagosome and targeting of this transport vesicle to the lysosome/late endosome for degradation. EPG5 is a large-sized metazoan protein proposed to serve as a tethering factor to enforce autophagosome-lysosome/late endosome fusion specificity, and its deficiency causes a severe multisystem disorder known as Vici syndrome. Here, we show that human EPG5 (hEPG5) adopts an extended "shepherd's staff" architecture. We find that hEPG5 binds preferentially to members of the GABARAP subfamily of human ATG8 proteins critical to autophagosome-lysosome fusion. The hEPG5-GABARAPs interaction, which is mediated by tandem LIR motifs that exhibit differential affinities, is required for hEPG5 recruitment to mitochondria during PINK1/Parkin-dependent mitophagy. Lastly, we find that the Vici syndrome mutation Gln336Arg does not affect the hEPG5's overall stability nor its ability to engage in interaction with the GABARAPs. Collectively, results from our studies reveal new insights into how hEPG5 recognizes mature autophagosome and establish a platform for examining the molecular effects of Vici syndrome disease mutations on hEPG5.
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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.