ArticleCell death and differentiation2019
Dclk1 in tuft cells promotes inflammation-driven epithelial restitution and mitigates chronic colitis.
Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Organoid Models of Colorectal Pathology: Do They Hold the Key to Personalized Medicine? A Systematic Review.Diseases of the colon and rectum · 2020Pooled it
- IRF7 signalling in tanycytes controls brain-body-immune response across the ovarian cycle.Nature metabolism · 2026Article
- Article
- Tuft cells protect against intestinal inflammation through histone deacetylase 3.Mucosal immunology · 2026Article
- Context-Dependent Modulation of Epithelial Barrier Integrity and Intestinal Permeability by Transcutaneous Auricular Vagus Nerve Stimulation in Two Preclinical Models Mimicking Ulcerative Colitis and Crohn's Disease: A Descriptive Analysis.International journal of molecular sciences · 2026Article
- Roles for specialized secretory epithelial cells in inflammatory bowel disease.Current opinion in gastroenterology · 2026Review
- Tuft cells contribute to the pathogenesis of human primary and experimental murine Sjögren's disease.Journal of dental sciences · 2026Article
- Renshen-Baidu-San restores epithelial-immune crosstalk and drives type 2 immune repair in ulcerative colitis: an integrated multi-omics study.Frontiers in immunology · 2026Article
- Mucosal kinase activity and inflammatory profiles in inflammatory bowel disease, and in relation to tofacitinib response.Journal of Crohn's & colitis · 2025Article
- Review
- DCLK1 isoform (DCLK1-S) as a critical player in promoting inflammation, tissue remodeling, and EMT in mouse models of colitis.PLoS pathogens · 2025Article
- Excretory/secretory products from Hymenolepis nana adult worms alleviate ulcerative colitis in mice via tuft/IL-13 signaling pathway.Parasites & vectors · 2025Article
- Balancing Regeneration and Resistance: Targeting DCLK1 to Mitigate Gastrointestinal Radiation Injury and Oncogenesis.Cancers · 2025Review
- Exogenous TSG-6 treatment alleviates DSS-induced colitis in mice by modulating Pou2f3 and promoting tuft cells differentiation.Molecular medicine (Cambridge, Mass.) · 2025Article
- Coevolutionary interplay: Helminths-trained immunity and its impact on the rise of inflammatory diseases.eLife · 2025Review
- Melatonin via MTNR1B regulates METTL3 to protect ileum cell differentiation.Inflammation · 2025Article
- Acute tuft cell ablation in mice induces malabsorption and alterations in secretory and immune cell lineages in the small intestine.Physiological reports · 2025Article
- Gut microbiota dysbiosis in inflammatory bowel disease: interaction with intestinal barriers and microbiota-targeted treatment options.Frontiers in cellular and infection microbiology · 2025Review
- The emerging role of intestinal stem cells in ulcerative colitis.Frontiers in medicine · 2025Review
- The role of the tuft cell-interleukin-25 axis in the pathogenesis of inflammatory bowel disease.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by defective intestinal barrier integrity toward the microbiota and epithelial damage. Double cortin-like kinase 1 (Dclk1), a marker of intestinal tuft cells, can regulate tissue regenerative responses, but its role in epithelial repair during bacterial-dependent chronic colitis is unclear. We addressed this question using our recently developed mouse model of spontaneous microbiota-dependent colitis induced by mucin-type O-glycan deficiency (DKO), which recapitulates most features of human UC. We generated DKO mice lacking intestinal epithelial Dclk1 (DKO;Dclk1
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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.