ArticleGut2021
SETDB1 is required for intestinal epithelial differentiation and the prevention of intestinal inflammation.
Article in Gut, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The trial behind it
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Who cites it
58 citing papers in PubMed, 86 citations in OpenAlex.
- Inflammatory bowel disease and breast cancer: epidemiological evidence, shared biology, and clinical management.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Review
- Article
- Argonaute 2 drives resistance to immune checkpoint inhibitors in immunorefractory non-small cell lung cancer.PLoS biology · 2026Article
- Oxidative stress affects intestinal health by inhibiting the differentiation of porcine intestinal epithelial cells through producing arachidonic acid.Science China. Life sciences · 2026Article
- G9a-mediated H3K9me2 orchestrates intestinal epithelial regeneration through epigenetic silencing of cell cycle-related genes.Nature communications · 2026Article
- The emerging paradigms of SETD family enzymes as epigenetic regulators of the immune response in inflammatory diseases.Frontiers in immunology · 2026Review
- Cutaneous Lupus Features Specialized Stromal Niches and Altered Retroelement Expression.The Journal of investigative dermatology · 2025Article
- Necroptotic cell death consequences and disease relevance.Nature immunology · 2025Review
- A loss-of-function human ADAR variant activates innate immune response and promotes bowel inflammation.Nature communications · 2025Article
- SETDB1-Mediated Chromatin Regulation in Intestinal Epithelial Cells During Intestinal Ischemia-Reperfusion Injury.Acta histochemica et cytochemica · 2025Article
- Patients with Irritable Bowel Syndrome Exhibit Aberrant Expression of Endogenous Retroviruses and SETDB1.Cells · 2025Article
- Targeting the Tumor Epigenetic Regulator SETDB1 for Tumor Therapy.Current cancer drug targets · 2025Review
- Mechanisms of Acetate in Alleviating SETDB1-Linked Neuroinflammation and Cognitive Impairment in a Mouse Model of OSA.Journal of inflammation research · 2025Article
- Mechanism of cell death and its application in the repair of inflammatory bowel disease by mesenchymal stem cells.Frontiers in immunology · 2025Review
- The role and intrinsic connection of cellular senescence and cell death in inflammatory bowel disease.Frontiers in cell and developmental biology · 2025Review
- Stem cell activity-coupled suppression of endogenous retrovirus governs adult tissue regeneration.Cell · 2024Article
- Epithelial NSD2 maintains FMO-mediated taurine biosynthesis to prevent intestinal barrier disruption.Clinical and translational medicine · 2024Article
- SETDB1 targeting SESN2 regulates mitochondrial damage and oxidative stress in renal ischemia-reperfusion injury.BMC biology · 2024Article
- Enhanced Transcription of Human Endogenous Retroviruses and TRIM28 Downregulation in Patients with Inflammatory Bowel Disease.Viruses · 2024Article
Corrections and comments
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Authors and funding
25 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe intestinal epithelium is a rapidly renewing tissue which plays central roles in nutrient uptake, barrier function and the prevention of intestinal inflammation. Control of epithelial differentiation is essential to these processes and is dependent on cell type-specific activity of transcription factors which bind to accessible chromatin. Here, we studied the role of SET Domain Bifurcated Histone Lysine Methyltransferase 1, also known as ESET (SETDB1), a histone H3K9 methyltransferase, in intestinal epithelial homeostasis and IBD.
designWe investigated mice with constitutive and inducible intestinal epithelial deletion of
resultsDeletion of intestinal epithelial
conclusionSETDB1 plays an essential role in intestinal epithelial homeostasis. Future work is required to investigate whether rare variants in
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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.