ArticleGut2013
MTG16 contributes to colonic epithelial integrity in experimental colitis.
Article in Gut, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Mtg16 NHR1 mutations cause defects in lymphopoiesis and the response to anemia.Experimental hematology · 2025Article
- MTG16 regulates colonic epithelial differentiation, colitis, and tumorigenesis by repressing E protein transcription factors.JCI insight · 2022Article
- The Transcription Co-Repressors MTG8 and MTG16 Regulate Exit of Intestinal Stem Cells From Their Niche and Differentiation Into Enterocyte vs Secretory Lineages.Gastroenterology · 2020Article
- Transcribed ultraconserved region (T-UCR) uc.261 expression is closely correlated with disease activity and intestinal permeability in Crohn's disease.Therapeutic advances in gastroenterology · 2019Article
- BVES is required for maintenance of colonic epithelial integrity in experimental colitis by modifying intestinal permeability.Mucosal immunology · 2018Article
- MTG16 is a tumor suppressor in colitis-associated carcinoma.JCI insight · 2017Article
- Ornithine decarboxylase regulates M1 macrophage activation and mucosal inflammation via histone modifications.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Emerging Roles of MTG16 in Cell-Fate Control of Hematopoietic Stem Cells and Cancer.Stem cells international · 2017Review
- Transcriptional Regulation by ATOH1 and its Target SPDEF in the Intestine.Cellular and molecular gastroenterology and hepatology · 2017Article
- Article
- The L-Arginine Transporter Solute Carrier Family 7 Member 2 Mediates the Immunopathogenesis of Attaching and Effacing Bacteria.PLoS pathogens · 2016Article
- The arachidonic acid metabolite 11β-ProstaglandinF2α controls intestinal epithelial healing: deficiency in patients with Crohn's disease.Scientific reports · 2016Article
- Loss of PHLPP protects against colitis by inhibiting intestinal epithelial cell apoptosis.Biochimica et biophysica acta · 2015Article
- Exacerbated experimental colitis in TNFAIP8-deficient mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Transcriptional corepressor MTG16 regulates small intestinal crypt proliferation and crypt regeneration after radiation-induced injury.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Deletion of cationic amino acid transporter 2 exacerbates dextran sulfate sodium colitis and leads to an IL-17-predominant T cell response.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- High-throughput multi-analyte Luminex profiling implicates eotaxin-1 in ulcerative colitis.PloS one · 2013Article
Corrections and comments
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Authors and funding
21 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveThe myeloid translocation genes (MTGs) are transcriptional corepressors with both Mtg8(-/-) and Mtgr1(-/-) mice showing developmental and/or differentiation defects in the intestine. We sought to determine the role of MTG16 in intestinal integrity.
methodsBaseline and stress induced colonic phenotypes were examined in Mtg16(-/-) mice. To unmask phenotypes, we treated Mtg16(-/-) mice with dextran sodium sulphate (DSS) or infected them with Citrobacter rodentium and the colons were examined for ulceration and for changes in proliferation, apoptosis and inflammation.
resultsMtg16(-/-) mice have altered immune subsets, suggesting priming towards Th1 responses. Mtg16(-/-) mice developed increased weight loss, diarrhoea, mortality and histological colitis and there were increased innate (Gr1(+), F4/80(+), CD11c(+) and MHCII(+); CD11c(+)) and Th1 adaptive (CD4) immune cells in Mtg16(-/-) colons after DSS treatment. Additionally, there was increased apoptosis and a compensatory increased proliferation in Mtg16(-/-) colons. Compared with wild-type mice, Mtg16(-/-) mice exhibited increased colonic CD4;IFN-γ cells in vehicle-treated and DSS-treated mice. Adoptive transfer of wild-type marrow into Mtg16(-/-) recipients did not rescue the Mtg16(-/-) injury phenotype. Isolated colonic epithelial cells from DSS-treated Mtg16(-/-) mice exhibited increased KC (Cxcl1) mRNA expression when compared with wild-type mice. Mtg16(-/-) mice infected with C rodentium had more severe colitis and greater bacterial colonisation. Last, MTG16 mRNA levels were reduced in human ulcerative colitis versus normal colon tissues.
conclusionsThese observations indicate that MTG16 is critical for colonocyte survival and regeneration in response to intestinal injury and provide evidence that this transcriptional corepressor regulates inflammatory recruitment in response to injury.
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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.