ArticleStem cell reports2015
Activated STAT5 confers resistance to intestinal injury by increasing intestinal stem cell proliferation and regeneration.
Article in Stem cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 67 citations in OpenAlex.
- STAT5A-RNF8 signaling regulates homologous recombination repair and cisplatin responsiveness in cervical cancer.Neoplasia (New York, N.Y.) · 2026Article
- Glycocholic acid inhibits TRIB3-ID1 axis to acelerate colitis progression via suppressing intestinal stem cell renewal.Nature communications · 2026Article
- A polymer that reinforces luminal barrier function and attenuates inflammation in murine colitis.Research square · 2026Article
- Tetrameric STAT5 regulates the formation of immune niche cells to protect stem cell regenerative repair against mucosal inflammation.Experimental & molecular medicine · 2026Article
- Development of Colonic Polyposis in a Woman With Chronic Myeloid Leukemia Treated With Dasatinib.Case reports in hematology · 2026Article
- Autophagy inhibition in intestinal stem cells favors enteroendocrine cell differentiation through Stat92E activity.Disease models & mechanisms · 2025Article
- CD133-Guided RNA Nanoparticle Delivery of FTO siRNA Impairs Leukemia Resistance to Tyrosine Kinase Inhibitor Therapy.RNA nanomed · 2025Article
- STAT Signature Dish: Serving Immunity with a Side of Dietary Control.Biomolecules · 2025Review
- Predictors of Efficacy of Janus Kinase Inhibitors in Patients Affected by Ulcerative Colitis.Journal of clinical medicine · 2024Review
- Discovery of a dual-acting inhibitor of interleukin-1β and STATs for the treatment of inflammatory bowel disease.RSC medicinal chemistry · 2024Article
- Monogenic deficiency in murine intestinal Cdc42 leads to mucosal inflammation that induces crypt dysplasia.Genes & diseases · 2024Article
- Article
- Human α-Defensin 5International journal of molecular sciences · 2023Article
- Mesenchymal Stem Cell-Derived Exosomes are Effective for Radiation Enteritis and Essential for the Proliferation and Differentiation of Lgr5Tissue engineering and regenerative medicine · 2023Article
- Article
- Chicken-Specific Kinome Analysis of Early Host Immune Signaling Pathways in the Cecum of Newly Hatched Chickens Infected WithFrontiers in cellular and infection microbiology · 2022Article
- JAK/STAT of all trades: linking inflammation with cancer development, tumor progression and therapy resistance.Carcinogenesis · 2021Article
- Epithelial wound healing in inflammatory bowel diseases: the next therapeutic frontier.Translational research : the journal of laboratory and clinical medicine · 2021Review
- Article
- Targeting JAK/STAT signaling pathways in treatment of inflammatory bowel disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Intestinal epithelial stem cells (IESCs) control the intestinal homeostatic response to inflammation and regeneration. The underlying mechanisms are unclear. Cytokine-STAT5 signaling regulates intestinal epithelial homeostasis and responses to injury. We link STAT5 signaling to IESC replenishment upon injury by depletion or activation of Stat5 transcription factor. We found that depletion of Stat5 led to deregulation of IESC marker expression and decreased LGR5(+) IESC proliferation. STAT5-deficient mice exhibited worse intestinal histology and impaired crypt regeneration after γ-irradiation. We generated a transgenic mouse model with inducible expression of constitutively active Stat5. In contrast to Stat5 depletion, activation of STAT5 increased IESC proliferation, accelerated crypt regeneration, and conferred resistance to intestinal injury. Furthermore, ectopic activation of STAT5 in mouse or human stem cells promoted LGR5(+) IESC self-renewal. Accordingly, STAT5 promotes IESC proliferation and regeneration to mitigate intestinal inflammation. STAT5 is a functional therapeutic target to improve the IESC regenerative response to gut injury.
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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.