Evidence map›Paper›PMID 22264340›Full record

ArticleGenome medicine2012

The balance of expression of PTPN22 splice forms is significantly different in rheumatoid arthritis patients compared with controls.

Marcus Ronninger, Yongjing Guo, Klementy Shchetynsky, Andrew Hill, Mohsen Khademi, Tomas Olsson, Padmalatha S Reddy, Maria Seddighzadeh, James D Clark, Lih-Ling Lin and 2 more

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In one paragraph

Article in Genome medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from 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.

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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. eLife · 2023
    Article
  3. AlteredDiagnostics (Basel, Switzerland) · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Conserved 33-kb haplotype in the MHC class III region regulates chronic arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  9. PTPN22: the archetypal non-HLA autoimmunity gene.Nature reviews. Rheumatology · 2014
    Review
  10. Article
  11. Review
  12. Article
  13. Genetics and epigenetics of rheumatoid arthritis.Nature reviews. Rheumatology · 2013
    Review
  14. Article
  15. 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

12 authors at 3 institutions in 2 countries.

Marcus RonningerDepartment of Medicine, Rheumatology Unit, CMM L8:04, Karolinska Institutet & Karolinska Universitetssjukhuset, Stockholm, S-17176, Sweden. marcus.ronninger@ki.se.
Yongjing Guo
Klementy Shchetynsky
Andrew Hill
Mohsen Khademi
Tomas Olsson
Padmalatha S Reddy
Maria Seddighzadeh
James D Clark
Lih-Ling Lin
Margot O'Toole
Leonid Padyukov
Karolinska University Hospital · SEPfizer (United States) · USKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe R620W variant in protein tyrosine phosphatase non-receptor 22 (PTPN22) is associated with rheumatoid arthritis (RA). The PTPN22 gene has alternatively spliced transcripts and at least two of the splice forms have been confirmed to encode different PTPN22 (LYP) proteins, but detailed information regarding expression of these is lacking, especially with regard to autoimmune diseases.

methodsWe have investigated the mRNA expression of known PTPN22 splice forms with TaqMan real-time PCR in relation to ZNF592 as an endogenous reference in peripheral blood cells from three independent cohorts with RA patients (n = 139) and controls (n = 111) of Caucasian origin. Polymorphisms in the PTPN22 locus (25 SNPs) and phenotypic data (gender, disease activity, ACPA and RF status) were used for analysis. Additionally, we addressed possible effects of methotrexate treatment on PTPN22 expression.

resultsWe found consistent differences in the expression of the PTPN22 splice forms in unstimulated peripheral blood mononuclear cells between RA patients and normal controls. This difference was more pronounced when comparing the ratio of splice forms and was not affected by methotrexate treatment.

conclusionsOur data show that RA patients and healthy controls have a shift in balance of expression of splice forms derived from the PTPN22 gene. This balance seems not to be caused by treatment and may be of importance during immune response due to great structural differences in the encoded PTPN22 proteins.

Identifiers

PMID22264340
PMCPMC3334550
OpenAlexW2112521208

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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.