ReviewAutophagy2015
ATG16L1: A multifunctional susceptibility factor in Crohn disease.
Review in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- Association between ATG16L1 gene polymorphism and the risk of Crohn's disease.The Journal of international medical research · 2017Pooled it
- A Developmental Perspective on the Intestinal Microbiota in Crohn's Disease.International journal of molecular sciences · 2026Review
- Canonical pathways and selective mechanisms of autophagy in inflammatory bowel disease.Advanced biotechnology · 2026Review
- Integrating multi-omics and multi-context QTL data with GWAS reveals the genetic architecture of complex traits and improves the discovery of risk genes.medRxiv : the preprint server for health sciences · 2026Article
- Interplay Between Dysregulated Immune System and the Footprints of Blood-Borne miRNAs in Treatment Naive Crohn's Disease and Ulcerative Colitis Patients.International journal of molecular sciences · 2025Article
- Distinct B Cell Subsets Changes as Potential Biomarkers of Response to Biologic Therapy in Crohn's Disease.International journal of molecular sciences · 2025Article
- The Role of Gut Microbiota in Gastrointestinal Immune Homeostasis and Inflammation: Implications for Inflammatory Bowel Disease.Biomedicines · 2025Review
- Shared Genetics in Celiac Disease and Inflammatory Bowel Disease Specify a Greater Role for Intestinal Epithelial Cells.International journal of molecular sciences · 2025Review
- Atg5 in microglia regulates sex-specific effects on postnatal neurogenesis in Alzheimer's disease.npj aging · 2025Article
- Multi-Ancestry Transcriptome-Wide Association Studies of Cognitive Function, White Matter Hyperintensity, and Alzheimer's Disease.International journal of molecular sciences · 2025Article
- MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Association between ATG16L1 rs2241880(T300A) and rs4663421 and ANCA‑associated vasculitis in the Guangxi population of China: Propensity score matching analysis.Biomedical reports · 2025Article
- Fundamental and emerging insights into innate and adaptive immunity in inflammatory bowel diseases.Frontiers in immunology · 2025Review
- Autophagy in inflammatory bowel disease: immunization, etiology, and therapeutic potential.Frontiers in immunology · 2025Review
- ATG16L1 promotes cell migration and invasion in high glucose-induced retinal capillary endothelial cells.Frontiers in medicine · 2025Article
- Intraperitoneal Administration of S100A8 Ameliorates Experimental Acute Colitis in Rats.Biology · 2024Article
- The Contribution of Genetic and Epigenetic Factors: An Emerging Concept in the Assessment and Prognosis of Inflammatory Bowel Diseases.International journal of molecular sciences · 2024Review
- Pharmacological induction of autophagy reduces inflammation in macrophages by degrading immunoproteasome subunits.PLoS biology · 2024Article
- IAPs and RIPK1 mediate LPS-induced cytokine production in healthy subjects and Crohn's disease.Clinical and experimental immunology · 2024Article
- Molecular Foundations of Inflammatory Diseases: Insights into Inflammation and Inflammasomes.Current issues in molecular biology · 2024Review
19 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
5 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic variations in the autophagic pathway influence genetic predispositions to Crohn disease. Autophagy, the major lysosomal pathway for degrading and recycling cytoplasmic material, constitutes an important homeostatic cellular process. Of interest, single-nucleotide polymorphisms in ATG16L1 (autophagy-related 16-like 1 [S. cerevisiae]), a key component in the autophagic response to invading pathogens, have been associated with an increased risk of developing Crohn disease. The most common and well-studied genetic variant of ATG16L1 (rs2241880; leading to a T300A conversion) exhibits a strong association with risk for developing Crohn disease. The rs2241880 variant plays a crucial role in pathogen clearance, resulting in imbalanced cytokine production, and is linked to other biological processes, such as the endoplasmic reticulum stress/unfolded protein response. In this review, we focus on the importance of ATG16L1 and its genetic variant (T300A) within the elementary biological processes linked to Crohn disease.
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What OpenQuestion holds
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.