ArticleNature communications2016
TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 112 citations in OpenAlex.
- Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Transcriptome-Wide Association Study for Inflammatory Bowel Disease Reveals Novel Candidate Susceptibility Genes in Specific Colon Subsites and Tissue Categories.Journal of Crohn's & colitis · 2022Pooled it
- AXL-dependent autophagy impairment differentiates monocyte-derived macrophages from Crohn's disease and intestinal tuberculosis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026Article
- Canonical pathways and selective mechanisms of autophagy in inflammatory bowel disease.Advanced biotechnology · 2026Review
- Phloretin as a Multitarget Neuroprotective Agent: Mechanistic Insights into the Modulation of Oxidative Stress, Inflammation, and Apoptosis.Neuromolecular medicine · 2026Review
- Genotype subtyping approach to identify unnoticed variants in diseases from GWAS data.BioData mining · 2026Article
- Golgi Membrane-Associated Degradation (GOMED), a New Intracellular Proteolysis Mechanism.Sub-cellular biochemistry · 2026Review
- The viral proteins of influenza A virus competitively bind to TRIM31 with MAVS to fine-tune the antiviral innate immunity.Journal of virology · 2025Article
- Bioinformatics analysis of the expression of TRIM31 mRNA and protein in pan-cancer tissues and their prognostic relevance.Scientific reports · 2025Article
- Discovery of Golgi membrane-associated degradation (GOMED) pathway: a focus on 15 years of ultrastructural analyses.Microscopy (Oxford, England) · 2025Review
- The Role of the Beclin1 Complex in Rab9-Dependent Alternative Autophagy.International journal of molecular sciences · 2025Review
- Atg7 in CD4Clinical and translational medicine · 2025Article
- Synthesis of Autotaxin-Inhibiting Lipid Nanoparticles to Regulate Autophagy and Inflammatory Responses in Activated Macrophages.Tissue engineering and regenerative medicine · 2025Article
- Article
- Review
- E3 ubiquitin ligase TRIM31 alleviates dopaminergic neurodegeneration by promoting proteasomal degradation of VDAC1 in Parkinson's Disease model.Cell death and differentiation · 2024Article
- Combined bacterial translocation and cholestasis aggravates liver injury by activation pyroptosis in obstructive jaundice.Heliyon · 2024Article
- Physiological functions of ULK1/2.Journal of molecular biology · 2024Review
- Reduction of DHHC5-mediated beclin 1 S-palmitoylation underlies autophagy decline in aging.Nature structural & molecular biology · 2024Article
- Multipronged regulation of autophagy and apoptosis: emerging role of TRIM proteins.Cellular & molecular biology letters · 2024Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is responsible for the bulk degradation of cytosolic constituents and plays an essential role in the intestinal epithelium by controlling beneficial host-bacterial relationships. Atg5 and Atg7 are thought to be critical for autophagy. However, Atg5- or Atg7-deficient cells still form autophagosomes and autolysosomes, and are capable of removing proteins or bacteria. Here, we report that human TRIM31 (tripartite motif), an intestine-specific protein localized in mitochondria, is essential for promoting lipopolysaccharide-induced Atg5/Atg7-independent autophagy. TRIM31 directly interacts with phosphatidylethanolamine in a palmitoylation-dependent manner, leading to induction of autolysosome formation. Depletion of endogenous TRIM31 significantly increases the number of intestinal epithelial cells containing invasive bacteria. Crohn's disease patients display TRIM31 downregulation. Human cytomegalovirus-infected intestinal cells show a decrease in TRIM31 expression as well as a significant increase in bacterial load, reversible by the introduction of wild-type TRIM31. We provide insight into an alternative autophagy pathway that protects against intestinal pathogenic bacterial infection.
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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.