ArticleAutophagy2018
The Vici syndrome protein EPG5 regulates intracellular nucleic acid trafficking linking autophagy to innate and adaptive immunity.
Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate immune activation.Nature communications · 2026Article
- Progressive neuroinflammation and deficits in motor function in a mouse model with an Epg5 pathogenic variant of Vici syndrome.Experimental & molecular medicine · 2026Article
- From chromatin to proteostasis: multilevel gene regulation in Mendelian diseases.Frontiers in epigenetics and epigenomics · 2026Review
- Epg5 links proteotoxic stress due to defective autophagic clearance and epileptogenesis inAutophagy · 2025Article
- An update on autophagy disorders.Journal of inherited metabolic disease · 2025Review
- Expanding the Spectrum of Immune Abnormalities in VICI Syndrome.Journal of clinical immunology · 2024Article
- Clinical Presentation and Molecular Characterization of 3 Patients with Vici Syndrome: Two Novel Variants in theMolecular syndromology · 2024Article
- Perinatal clinical course of Vici syndrome associated with novelBMJ case reports · 2024Article
- New insights into the genetic predisposition of brucellosis and its effect on the gut and vaginal microbiota in goats.Scientific reports · 2023Article
- Genome-Wide Re-Sequencing Data Reveals the Population Structure and Selection Signatures of Tunchang Pigs in China.Animals : an open access journal from MDPI · 2023Article
- Article
- PI4K2A deficiency causes innate error in intracellular trafficking with developmental and epileptic-dyskinetic encephalopathy.Annals of clinical and translational neurology · 2022Article
- The molecular regulation of autophagy in antimicrobial immunity.Journal of molecular cell biology · 2022Article
- Human platelets display dysregulated sepsis-associated autophagy, induced by altered LC3 protein-protein interaction of the Vici-protein EPG5.Autophagy · 2022Article
- TFG is required for autophagy flux and to prevent endoplasmic reticulum stress in CH12 B lymphoma cells.Autophagy · 2021Article
- Pathogenic Single Nucleotide Polymorphisms on Autophagy-Related Genes.International journal of molecular sciences · 2020Review
- A current view of molecular dissection in autophagy machinery.Journal of physiology and biochemistry · 2020Review
- TFEB-dependent induction of thermogenesis by the hepatocyte SLC2A inhibitor trehalose.Autophagy · 2018Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vici syndrome is a human inherited multi-system disorder caused by recessive mutations in EPG5, encoding the EPG5 protein that mediates the fusion of autophagosomes with lysosomes. Immunodeficiency characterized by lack of memory B cells and increased susceptibility to infection is an integral part of the condition, but the role of EPG5 in the immune system remains unknown. Here we show that EPG5 is indispensable for the transport of the TLR9 ligand CpG to the late endosomal-lysosomal compartment, and for TLR9-initiated signaling, a step essential for the survival of human memory B cells and their ultimate differentiation into plasma cells. Moreover, the predicted structure of EPG5 includes a membrane remodeling domain and a karyopherin-like domain, thus explaining its function as a carrier between separate vesicular compartments. Our findings indicate that EPG5, by controlling nucleic acids intracellular trafficking, links macroautophagy/autophagy to innate and adaptive immunity.
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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.