ArticleJournal of clinical immunology2010
Inhibitor IkappaBalpha promoter functional polymorphisms in patients with rheumatoid arthritis.
Article in Journal of clinical immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 15 citations in OpenAlex.
- Common Polymorphisms in the NFKBIA Gene and Cancer Susceptibility: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015Pooled it
- Polymorphisms in the CTLA-4 gene and rheumatoid arthritis susceptibility: a meta-analysis.Journal of clinical immunology · 2012Pooled it
- GADD45a and GADD45b Genes in Rheumatoid Arthritis and Systemic Lupus Erythematosus Patients.Journal of clinical medicine · 2019Article
- Association between genetic polymorphism in NFKB1 and NFKBIA and coronary artery disease in a Chinese Han population.International journal of clinical and experimental medicine · 2015Article
- Inhibitor IκBα promoter functional polymorphisms in patients with multiple sclerosis.Molecular biology reports · 2014Article
- Gender-specific association of NFKBIA promoter polymorphisms with the risk of sporadic colorectal cancer.Medical oncology (Northwood, London, England) · 2013Article
- Effects of NFKB1 and NFKBIA gene polymorphisms on hepatocellular carcinoma susceptibility and clinicopathological features.PloS one · 2013Article
- Genetic variants in the NF-κB signaling pathway (NFKB1, NFKBIA, NFKBIZ) and risk of critical outcome among COVID-19 patients.Human immunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionRheumatoid arthritis (RA) is a chronic inflammation disease that may involve extra-articular organs in addition to joints. Many proinflammatory cytokines are involved in the inflammatory process of RA. IkappaBalpha conjugates with NF-kappaB and is a key player in regulation of the inflammatory process. We carried out experiments to define the effect of different promoter polymorphisms on the transcriptional activities of IkappaBalpha promoter and the development of RA.
methodsDifferent IkappaBalpha promoter reporters were constructed and were examined in human mononuclear cells, THP-1 cells. One hundred forty patients and 115 healthy controls were recruited from the Kaohsiung Medical University Hospital.
resultsThe activities of IkappaBalpha promoter constructs with -826C, -550A, -519T, and -826T, -550A, -519T genotypes were expressed at one half the activity level of other constructs. Promoter constructs containing the sites -550A/T and -519T had a reduced risk of rheumatoid arthritis. The odds ratio of -826C/T genotype was significantly associated with an increase of risk in causing rheumatoid arthritis, whereas -826T/T genotype was associated only with a slightly increased risk of RA, but without statistical significance (odds ratio = 1.2; 95% confidence interval, 0.4-3.8).
conclusionThe increase of T allele was associated with a significant increased risk and the tendency to the pathogenesis of RA. The association between IkappaBalpha promoter polymorphisms and disease severity of rheumatoid arthritis is partly due to different transcriptional activities of IkappaBalpha promoter and the activation of NF-kappaB.
Indexed as
Identifiers
What OpenQuestion holds
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.