ArticleGut2002
Activation of signal transducer and activator of transcription (STAT) 1 in human chronic inflammatory bowel disease.
Article in Gut, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 210 citations in OpenAlex.
- Trial
- TNK1 is a targetable JAK-independent driver of STAT signaling and inflammation.Genes & development · 2026Article
- Threonine phosphorylation of STAT1 safeguards gut epithelial integrity and restricts interferon-mediated cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- State-of-the-Art Evidence for Clinical Outcomes and Therapeutic Implications of Janus Kinase Inhibitors in Moderate-to-Severe Ulcerative Colitis: A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Intensive Granulocyte and Monocyte Adsorptive Apheresis Plus Upadacitinib for Induction Treatment of Refractory Crohn's Disease.Journal of clinical medicine research · 2025Article
- Exploration of JAK/STAT pathway activation in ulcerative colitis reveals sex-dependent activation of JAK2/STAT3 in the inflammatory response.Frontiers in immunology · 2025Observational
- Cimifugin ameliorates ulcerative colitis-related lung injury by modulating the JAK1/STAT1 signaling pathway and macrophage M1 polarization.Frontiers in immunology · 2025Article
- JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025Review
- Article
- Histological Outcomes and JAK-STAT Signalling in Ulcerative Colitis Patients Treated with Tofacitinib.Journal of Crohn's & colitis · 2024Article
- CBX3 antagonizes IFNγ/STAT1/PD-L1 axis to modulate colon inflammation and CRC chemosensitivity.EMBO molecular medicine · 2024Article
- Efficacy and Safety of Upadacitinib Plus Intensive Granulocyte and Monocyte Adsorptive Apheresis as Induction for Intractable Ulcerative Colitis.Journal of clinical medicine research · 2024Article
- Discovery of a dual-acting inhibitor of interleukin-1β and STATs for the treatment of inflammatory bowel disease.RSC medicinal chemistry · 2024Article
- A proteomic insight reveals the role of food-associatediScience · 2023Article
- The Antioxidant Properties ofAntioxidants (Basel, Switzerland) · 2023Article
- Article
- The IL-10 receptor inhibits cell extrinsic signals necessary for STAT1-dependent macrophage accumulation during colitis.Mucosal immunology · 2023Article
- The landscape of immune dysregulation in Crohn's disease revealed through single-cell transcriptomic profiling in the ileum and colon.Immunity · 2023Article
- T Cell Energy Metabolism Is a Target of Glucocorticoids in Mice, Healthy Humans, and MS Patients.Cells · 2023Article
- Article
33 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
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreased expression of proinflammatory cytokines, including tumour necrosis factor alpha, interleukin 6, and interferon gamma, as well as activation of proinflammatory signalling molecules such as nuclear factor kappa B, is characteristic of inflammatory bowel disease (IBD).
aimsTo investigate expression and activation of signal transducer and activator of transcription (STAT) 1 in patients with IBD. PATIENTS: Patients with active IBD (n=42), disease specificity controls (n=8), and normal controls (n=12) were investigated.
methodsExpression and activation of STAT1 were assessed by western blotting and electrophoretic mobility shift assays in extracts of endoscopic colonic biopsies. Cellular localisation was determined by immunohistochemistry.
resultsWestern blots and immunohistochemical staining revealed an increase in STAT1 expression and activation in mucosal samples from ulcerative colitis and to a lesser extend in Crohn's disease patients. High levels of suppressor of cytokine signalling (SOCS)-3 expression, an inhibitor of STAT activation, were observed in Crohn's disease patients and normal controls in western blot experiments whereas no differences were observed for SOCS-1 expression. Phosphorylated (p) STAT1 was mainly detected in monocytic cells and neutrophils in the inflamed mucosa. Induction of remission by systemic glucocorticoids led to a decrease in levels of pSTAT1. In vitro studies indicated a direct effect of steroid treatment on STAT1 activation.
conclusionsExpression and activation of STAT1 are predominantly heightened in ulcerative colitis and may therefore play an important role in the pathophysiology of colonic inflammation.
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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.