Evidence map›Paper›PMID 11828340›Full record

ArticleAmerican journal of human genetics2002

Association between single-nucleotide polymorphisms in selectin genes and immunoglobulin A nephropathy.

Takashi Takei, Aritoshi Iida, Kosaku Nitta, Toshihiro Tanaka, Yozo Ohnishi, Ryo Yamada, Shiro Maeda, Tatsuhiko Tsunoda, Sachiyo Takeoka, Kyoko Ito and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of human genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 78 citations in OpenAlex.

  1. Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024
    Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Polymorphisms in host genes encoding NOSII, C-reactive protein, and adhesion molecules thrombospondin and E-selectin are risk factors for Plasmodium falciparum malaria in India.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2015
    Article
  8. Development of Animal Models of Human IgA Nephropathy.Drug discovery today. Disease models · 2014
    Article
  9. Article
  10. Article
  11. Article
  12. Development of a model of early-onset IgA nephropathy.Journal of the American Society of Nephrology : JASN · 2012
    Article
  13. Article
  14. Genetics and immunopathogenesis of IgA nephropathy.Clinical reviews in allergy & immunology · 2011
    Review
  15. Article
  16. IL5RA and TNFRSF6B gene variants are associated with sporadic IgA nephropathy.Journal of the American Society of Nephrology : JASN · 2008
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

22 authors at 5 institutions in 1 country.

Takashi TakeiHuman Genome Center, The Institute of Medical Science, University of Tokyo, Tokyo Women's Medical University, Tokyo, Japan.
Aritoshi Iida
Kosaku Nitta
Toshihiro Tanaka
Yozo Ohnishi
Ryo Yamada
Shiro Maeda
Tatsuhiko Tsunoda
Sachiyo Takeoka
Kyoko Ito
Kazuho Honda
Keiko Uchida
Ken Tsuchiya
Yasushi Suzuki
Tomoaki Fujioka
Takashi Ujiie
Yutaka Nagane
Satoru Miyano
Ichiei Narita
Fumitake Gejyo
Hiroshi Nihei
Yusuke Nakamura
Tokyo Women's Medical University · JPIwate Medical University · JPNiigata University · JPIwate Prefectural Central Hospital · JPRIKEN · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although intensive efforts have been undertaken to elucidate the genetic background of immunoglobulin A nephropathy (IgAN), genetic factors associated with the pathogenesis of this disease are still not well understood. We designed a case-control association study that was based on linkage disequilibrium among single-nucleotide polymorphisms (SNPs) in the selectin gene cluster on chromosome 1q24-25, and we found two SNPs in the E-selectin gene (SELE8 and SELE13) and six SNPs in the L-selectin gene (SELL1, SELL4, SELL5, SELL6, SELL10, and SELL11) that were significantly associated with IgAN in Japanese patients. All eight SNPs were in almost complete linkage disequilibrium. SELE8 and SELL10 caused amino acid substitutions from His to Tyr and from Pro to Ser (chi2=9.02, P=.0026, odds ratio = 2.73 [95% confidence interval [CI] 1.38--5.38] for His-to-Tyr substitutions; chi2=17.4, P=.000031, odds ratio = 3.61 [95% CI 1.91--6.83] for Pro-to-Ser substitutions), and SELL1 could affect promoter activity of the L-selectin gene (chi2=19.5, P=.000010, odds ratio = 3.77 [95% CI 2.02--7.05]). The TGT haplotype at these three loci was associated significantly with IgAN (chi2=18.67, P=.000016, odds ratio = 1.88 [95% CI 1.41--2.51]). Our results suggest that these eight SNPs in selectin genes may be useful for screening populations susceptible to the IgAN phenotype that involves interstitial infiltration.

Indexed as

Case-Control StudiesChromosomes, Human, Pair 1E-SelectinGenetic Predisposition to DiseaseGenetic TestingGlomerulonephritis, IGAHaplotypesHumansJapanLinkage DisequilibriumL-SelectinMultigene FamilyOdds RatioPolymorphism, Single NucleotidePromoter Regions, GeneticE-SelectinL-Selectin

Identifiers

PMID11828340
PMCPMC384956
OpenAlexW2014559338

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Registered trials

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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.