Evidence map›Paper›PMID 23028356›Full record

ArticlePLoS genetics2012

Functional variants in NFKBIE and RTKN2 involved in activation of the NF-κB pathway are associated with rheumatoid arthritis in Japanese.

Keiko Myouzen, Yuta Kochi, Yukinori Okada, Chikashi Terao, Akari Suzuki, Katsunori Ikari, Tatsuhiko Tsunoda, Atsushi Takahashi, Michiaki Kubo, Atsuo Taniguchi and 9 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Lupus susceptibility geneScience advances · 2024
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  8. Genetics of rheumatoid arthritis.Seminars in immunopathology · 2022
    Review
  9. Lipidomic Profiling in Synovial Tissue.Frontiers in medicine · 2022
    Review
  10. The Role of Oxidative Stress in Intervertebral Disc Degeneration.Oxidative medicine and cellular longevity · 2022
    Review
  11. Neurology(R) neuroimmunology & neuroinflammation · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors at 4 institutions in 1 country.

Keiko MyouzenLaboratory for Autoimmune Diseases, Center for Genomic Medicine, RIKEN, Yokohama, Japan.
Yuta Kochi
Yukinori Okada
Chikashi Terao
Akari Suzuki
Katsunori Ikari
Tatsuhiko Tsunoda
Atsushi Takahashi
Michiaki Kubo
Atsuo Taniguchi
Fumihiko Matsuda
Koichiro Ohmura
Shigeki Momohara
Tsuneyo Mimori
Hisashi Yamanaka
Naoyuki Kamatani
Ryo Yamada
Yusuke Nakamura
Kazuhiko Yamamoto
Kyoto University · JPRIKEN Center for Integrative Medical Sciences · JPTokyo Women's Medical University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis is an autoimmune disease with a complex etiology, leading to inflammation of synovial tissue and joint destruction. Through a genome-wide association study (GWAS) and two replication studies in the Japanese population (7,907 cases and 35,362 controls), we identified two gene loci associated with rheumatoid arthritis susceptibility (NFKBIE at 6p21.1, rs2233434, odds ratio (OR) = 1.20, P = 1.3 × 10(-15); RTKN2 at 10q21.2, rs3125734, OR = 1.20, P = 4.6 × 10(-9)). In addition to two functional non-synonymous SNPs in NFKBIE, we identified candidate causal SNPs with regulatory potential in NFKBIE and RTKN2 gene regions by integrating in silico analysis using public genome databases and subsequent in vitro analysis. Both of these genes are known to regulate the NF-κB pathway, and the risk alleles of the genes were implicated in the enhancement of NF-κB activity in our analyses. These results suggest that the NF-κB pathway plays a role in pathogenesis and would be a rational target for treatment of rheumatoid arthritis.

Indexed as

Arthritis, RheumatoidI-kappa B ProteinsIntracellular Signaling Peptides and ProteinsProto-Oncogene ProteinsGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansJapanNF-kappa BPolymorphism, Single NucleotideSignal TransductionI-kappa B ProteinsIntracellular Signaling Peptides and ProteinsNF-kappa BNFKBIE protein, humanProto-Oncogene ProteinsRTKN2 protein, human

Identifiers

PMID23028356
PMCPMC3441678
OpenAlexW2104982663

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.