ArticlePloS one2014
Functional effect of polymorphisms in the promoter of TNFAIP3 (A20) in acute pancreatitis in the Han Chinese population.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Meta-analysis and field synopsis of genetic variants associated with the risk and severity of acute pancreatitis.BJS open · 2020Pooled it
- Whole exome sequencing reveals aniMetaOmics · 2025Article
- Article
- No association of eight TNFAIP3 single nucleotide variants to rheumatoid arthritis in Mexicans.Molecular biology reports · 2022Article
- Fire in the belly: A scoping review of the immunopathological mechanisms of acute pancreatitis.Frontiers in immunology · 2022Article
- Genetic Polymorphisms: A Novel Perspective on Acute Pancreatitis.Gastroenterology research and practice · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe zinc finger protein A20 is an important negative regulator of inflammation; polymorphisms in the corresponding gene, TNFAIP3, have been reported to be associated with several inflammation diseases. However, only a few studies have focused on the relationship between TNFAIP3 polymorphisms and acute pancreatitis (AP).
methodsWe enrolled 201 healthy controls and 190 acute pancreatitis patients (including 47 systemic inflammatory response syndrome patients) for this study and used DNA sequencing to investigate polymorphisms in the TNFAIP3 promoter. The functional effects of these variants on transcriptional activity, A20 expression, NF-κB activity, and TNF-α and IL-1β levels, after in vitro lipopolysaccharide stimulation, were assessed.
resultsTwo SNPs (rs59693083 and rs5029924) in the TNFAIP3 promoter were selected based on bioinformatic analysis. Neither of these SNPs was associated with susceptibility to AP; however, acute pancreatitis patients who possessed the T allele of rs5029924 were more likely to experience systemic inflammatory response syndrome. Moreover, rs5029924 was found to affect TNFAIP3 promoter activity. After lipopolysaccharide stimulation, the expression of A20 protein significantly decreased, while the activity of NF-κB and the production of TNF-α and IL-1β significantly increased in whole blood leukocytes from subjects with the T allele.
conclusionThe rs5029924 polymorphism in the TNFAIP3 promoter may alter the risk of systemic inflammatory response syndrome in acute pancreatitis patients by influencing the expression of A20 protein.
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