ArticleDevelopment (Cambridge, England)2002
The zinc-finger transcription factor Klf4 is required for terminal differentiation of goblet cells in the colon.
Article in Development (Cambridge, England), 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 340 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
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.
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Who cites it
340 citing papers in PubMed, 579 citations in OpenAlex.
- Endothelial KLF4 depletion drives age-related neurovascular dysfunction and neuropsychiatric impairment.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Spatial transcriptomic analysis of foveolar-type gastric adenoma with raspberry-like appearance.Virchows Archiv : an international journal of pathology · 2026Article
- Villification of the intestinal epithelium is driven by Foxl1 through activation of PDGFRα and BMPs.Nature communications · 2026Article
- From mucus secretion to immune surveillance: the evolving roles of goblet cells in intestinal homeostasis and inflammation.Frontiers in immunology · 2026Review
- Article
- KRT6A and KRT17 Mark Distinct Stem Cell Populations in the Adult Palpebral Conjunctiva and Meibomian Gland.Cells · 2025Article
- Downregulation of Enteroendocrine Genes Predicts Survival in Colon Cancer: A Bioinformatics-Based Analysis.International journal of molecular sciences · 2025Article
- The role and mechanism of transcription factor KLF4 in regulating mitochondrial damage and apoptosis by activating chondrocyte autophagy in osteoarthritis.Scientific reports · 2025Article
- Review
- Hemodynamic forces prevent myxomatous valve disease in mice through KLF2/4 signaling.The Journal of clinical investigation · 2025Article
- Long-term consumption of moderate amounts of sucrose-sweetened drinks disrupts intestinal barrier function by impairing goblet cell differentiation.Cell and tissue research · 2025Article
- Loss of mucin 2 and MHC II molecules causes rare resistance to murine RV infection.Journal of virology · 2025Article
- GLP-1-based therapies for type 2 diabetes: from single, dual and triple agonists to endogenous GLP-1 production and L-cell differentiation.Diabetology & metabolic syndrome · 2025Review
- NKX2.2 and KLF4 cooperate to regulate α-cell identity.Genes & development · 2025Article
- Article
- KLF feedback loops in innate immunity.Frontiers in immunology · 2025Review
- Article
- A secreted helminth microRNA suppresses gastrointestinal cell differentiation required for innate immunity.Frontiers in immunology · 2025Article
- Downregulated KLF4, induced by m6A modification, aggravates intestinal barrier dysfunction in inflammatory bowel disease.Cellular and molecular life sciences : CMLS · 2024Article
- Review
280 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
7 authors at 2 institutions in 1 country.
Funding
Abstract
Klf4 (formerly GKLF) is a zinc-finger transcription factor expressed in the epithelia of the skin, lungs, gastrointestinal tract and several other organs. In vitro studies have suggested that Klf4 plays an important role in cell proliferation and/or differentiation. Mice homozygous for a null mutation in Klf4 die within 15 hours of birth and show selective perturbation of late-stage differentiation structures in the epidermis, but the function of Klf4 in the gastrointestinal tract has not been investigated. To address this issue, we have generated Klf4(-/-) mice by homologous recombination in embryonic stem cells. In this study, we provide the first in vivo evidence that Klf4 is a goblet cell-specific differentiation factor in the colon. Klf4(-/-) mice exhibit normal cell proliferation and cell death rates in the colon on postnatal day 1. However, Klf4(-/-) mice demonstrate a 90% decrease in the number of goblet cells in the colon, show abnormal expression of the goblet cell-specific marker Muc2 by in situ hybridization, have abnormal staining of the colonic epithelium with Alcian Blue for acidic mucins, and lack normal goblet cell morphology by ultrastructural analysis. All other epithelial cell types are present in the colon of Klf4(-/-) mice. In summary, Klf4 plays a crucial role in colonic epithelial cell differentiation in vivo.
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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.