ArticlePloS one2013
NF-kappaB mediated transcriptional repression of acid modifying hormone gastrin.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
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- RANKL coordinates multiple osteoclastogenic pathways by regulating expression of ubiquitin ligase RNF146.The Journal of clinical investigation · 2017Article
- Dexamethasone downregulates expression of carbonic anhydrase IX via HIF-1α and NF-κB-dependent mechanisms.International journal of oncology · 2016Article
- Dual Activation of TRIF and MyD88 Adaptor Proteins by Angiotensin II Evokes Opposing Effects on Pressure, Cardiac Hypertrophy, and Inflammatory Gene Expression.Hypertension (Dallas, Tex. : 1979) · 2015Article
- PKCζ Promotes Breast Cancer Invasion by Regulating Expression of E-cadherin and Zonula Occludens-1 (ZO-1) via NFκB-p65.Scientific reports · 2015Article
- To be or not to be: The host genetic factor and beyond in Helicobacter pylori mediated gastro-duodenal diseases.World journal of gastroenterology · 2015Review
- Delta-tocotrienol suppresses radiation-induced microRNA-30 and protects mice and human CD34+ cells from radiation injury.PloS one · 2015Article
- Investigation of NF-κB1 and NF-κBIA gene polymorphism in non-small cell lung cancer.BioMed research international · 2014Article
- Computational Modeling of Gene-Specific Transcriptional Repression, Activation and Chromatin Interactions in Leukemogenesis by LASSO-Regularized Logistic Regression.IEEE/ACM transactions on computational biology and bioinformaticsArticle
- NF-κB p65 regulates hepatic lipogenesis by promoting nuclear entry of ChREBP in response to a high carbohydrate diet.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori is a major pathogen associated with the development of gastroduodenal diseases. It has been reported that H. pylori induced pro-inflammatory cytokine IL1B is one of the various modulators of acid secretion in the gut. Earlier we reported that IL1B-activated NFkB down-regulates gastrin, the major hormonal regulator of acid secretion. In this study, the probable pathway by which IL1B induces NFkB and affects gastrin expression has been elucidated. IL1B-treated AGS cells showed nine-fold activation of MyD88 followed by phosphorylation of TAK1 within 15 min of IL1B treatment. Furthermore, it was observed that activated TAK1 significantly up-regulates the NFkB subunits p50 and p65. Ectopic expression of NFkB p65 in AGS cells resulted in about nine-fold transcriptional repression of gastrin both in the presence and absence of IL1B. The S536A mutant of NFkB p65 is significantly less effective in repressing gastrin. These observations show that a functional NFkB p65 is important for IL1B-mediated repression of gastrin. ChIP assays revealed the presence of HDAC1 and NFkB p65 along with NCoR on the gastrin promoter. Thus, the study provides mechanistic insight into the IL1B-mediated gastrin repression via NFkB.
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