ArticleScientific reports2017
Altered expression of Tumor Necrosis Factor Alpha -Induced Protein 3 correlates with disease severity in Ulcerative Colitis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
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- TNIP3 Attenuates Colitis by Inhibiting the TAB1/NF-κB/NLRP3 Signaling Pathway in Macrophages.Digestive diseases and sciences · 2026Article
- Functional changes in the gut microbiota are associated with the intestinal phenotype in A20 haploinsufficiency.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026Article
- A20 Facilitates Oxaliplatin Sensitivity in Colorectal Cancer Through Monoubiquitylation of IKK-β.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Co-Occurrence ofInternational journal of molecular sciences · 2025Article
- Inflammatory Gene Panel Guiding the Study of Genetics in Inflammatory Bowel Disease.Molecular diagnosis & therapy · 2024Review
- Microbial signals, MyD88, and lymphotoxin drive TNF-independent intestinal epithelial tissue damage.The Journal of clinical investigation · 2022Article
- Serum Proteomic Analysis of Cannabis Use Disorder in Male Patients.Molecules (Basel, Switzerland) · 2021Article
- Exploring the five different genes associated with PKCα in bladder cancer based on gene expression microarray.Journal of cellular and molecular medicine · 2021Article
- The Role of E3 Ubiquitin Ligases and Deubiquitinases in Inflammatory Bowel Disease: Friend or Foe?Frontiers in immunology · 2021Review
- Proteomics-Based Evidence for a Pro-Oncogenic Role of ESRP1 in Human Colorectal Cancer Cells.International journal of molecular sciences · 2020Article
- Investigation of Potential Genetic Biomarkers and Molecular Mechanism of Ulcerative Colitis Utilizing Bioinformatics Analysis.BioMed research international · 2020Article
- miR-125b and miR-223 Contribute to Inflammation by Targeting the Key Molecules of NFκB Pathway.Frontiers in medicine · 2019Article
- Identification of functional missense single-nucleotide polymorphisms inJournal of clinical and translational science · 2018Article
- On cell death in the intestinal epithelium and its impact on gut homeostasis.Current opinion in gastroenterology · 2018Review
- A20 and ABIN-1 synergistically preserve intestinal epithelial cell survival.The Journal of experimental medicine · 2018Article
- Identification and analysis of key genes associated with ulcerative colitis based on DNA microarray data.Medicine · 2018Article
- Effects of Sepantronium Bromide (YM-155) on the Whole Transcriptome of MDA-MB-231 Cells: Highlight on Impaired ATR/ATM Fanconi Anemia DNA Damage Response.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ulcerative colitis (UC), an inflammatory disorder of the colon arises from dysregulated immune response towards gut microbes. Transcription factor NFκB is a major regulatory component influencing mucosal inflammation. We evaluated expression of Tumor Necrosis Factor Alpha Induced Protein3 (TNFAIP3), the inhibitor of NFκB activation and its associated partners ITCH, RNF11 and Tax1BP1 in inflamed mucosa of UC patients. We found highly significant up-regulated mRNA expression of TNFAIP3 that negatively correlated with disease activity in UC. mRNA levels of ITCH, RNF11 and Tax1BP1 were significantly down-regulated. Significant positive correlation with disease activity was noted for Tax1BP1. All four genes showed significant down-regulation at protein level. mRNA levels of inducers of TNFAIP3 expression, NFκB p65 subunit and MAST3 was determined. There was significant increase in p65 mRNA expression and down-regulated MAST3 expression. This suggested that increase in NFκB expression regulates TNFAIP3 levels. Deficiency of TNFAIP3 expression resulted in significant up-regulation of NFκB p65 sub-unit as well as its downstream genes such as iNOS, an inflammatory marker, inhibitors of apoptosis like cIAP2 and XIAP and mediators of anti-apoptotic signals TRAF1 and TRAF2. Taken together, decreased expression of TNFAIP3 and its partners contribute to inflammation and up-regulation of apoptosis inhibitors that may create microenvironment for colorectal cancer.
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