ArticleInternational journal of clinical and experimental pathology2014
Role of far upstream element binding protein 1 in colonic epithelial disruption during dextran sulphate sodium-induced murine colitis.
Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Cell-type-resolved genetic regulatory variation shapes inflammatory bowel disease risk.medRxiv : the preprint server for health sciences · 2025Article
- FUBP1 in human cancer: Characteristics, functions, and potential applications.Translational oncology · 2024Review
- The transcriptional regulator FUBP1 influences disease outcome in murine and human myeloid leukemia.Leukemia · 2019Article
- Prophylactic TNF blockade uncouples efficacy and toxicity in dual CTLA-4 and PD-1 immunotherapy.Nature · 2019Article
- The master regulator FUBP1: its emerging role in normal cell function and malignant development.Cellular and molecular life sciences : CMLS · 2019Review
- MicroRNA-206 is involved in the pathogenesis of ulcerative colitis via regulation of adenosine A3 receptor.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimIntestinal epithelial barrier is essential for maintaining normal intestinal homeostasis; its breakdown leads to chronic inflammatory pathologies, such as inflammatory bowel diseases. Far upstream element binding protein 1 (FBP1) has been reported to play an important role in cell apoptosis and proliferation. We aimed to investigate the expression and the role of FBP1 in dextran sodium sulphate (DSS)-induced experimental colitis.
methodsMice experimental colitis model was established by administration of DSS, and the expression and localization of FBP1 was examined using Western blot and immunohistochemistry. Colon epithelial cell line HT-29 was used to determine the role of FBP1. In vitro study, the expression of FBP1 was determined in HT-29 cells stimulated with tumor necrosis factor α (TNF-α). HT-29 cells were transfected with FBP1 siRNA and then measured for viability.
resultsSignificant decreasing of FBP1 expression was found in mice colitis. In addition, FBP1 was cleaved and translocated from nucleus to cytoplasm during apoptosis. Downregulated expression of FBP1 induced cell cycle arrest.
conclusionsWe demonstrate that apoptosis-mediated cleavage of FBP1 and its decreased expression in epithelial cells induces cell cycle arrest, which may play an important role in colonic epithelial disruption.
Indexed as
Identifiers
24966911PMC4069948W2216979982What 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.