Evidence map›Paper›PMID 25901943›Full record

ArticlePloS one2015

Integrative omics analysis of rheumatoid arthritis identifies non-obvious therapeutic targets.

John W Whitaker, David L Boyle, Beatrix Bartok, Scott T Ball, Steffen Gay, Wei Wang, Gary S Firestein

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  5. Article
  6. Article
  7. Frontiers in genetics · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Cell-Free DNA in Rheumatoid Arthritis.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Review
  15. Review
  16. Observational
  17. Article
  18. Review
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

John W WhitakerDepartment of Chemistry and Biochemistry, University of California San Diego, La Jolla, California, United States of America; Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, California, United States of America.
David L BoyleDivision of Rheumatology, Allergy and Immunology, University of California San Diego, La Jolla, California, United States of America.
Beatrix BartokDivision of Rheumatology, Allergy and Immunology, University of California San Diego, La Jolla, California, United States of America.
Scott T BallDepartment of Orthopaedics, University of California San Diego School of Medicine, La Jolla, California, United States of America.
Steffen GayDepartment of Rheumatology, University Hospital Zürich, CH-8091, Zurich, Switzerland.
Wei WangDepartment of Chemistry and Biochemistry, University of California San Diego, La Jolla, California, United States of America; Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, California, United States of America.
Gary S FiresteinDivision of Rheumatology, Allergy and Immunology, University of California San Diego, La Jolla, California, United States of America.
University of California, San Diego · USUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Identifying novel therapeutic targets for the treatment of disease is challenging. To this end, we developed a genome-wide approach of candidate gene prioritization. We independently collocated sets of genes that were implicated in rheumatoid arthritis (RA) pathogenicity through three genome-wide assays: (i) genome-wide association studies (GWAS), (ii) differentially expression in RA fibroblast-like synoviocytes (FLS), and (iii) differentially methylation in RA FLS. Integrated analysis of these complementary data sets identified a significant enrichment of multi-evidence genes (MEGs) within pathways relating to RA pathogenicity. One MEG is Engulfment and Cell Motility Protein-1 (ELMO1), a gene not previously considered as a therapeutic target in RA FLS. We demonstrated in RA FLS that ELMO1 is: (i) expressed, (ii) promotes cell migration and invasion, and (iii) regulates Rac1 activity. Thus, we created links between ELMO1 and RA pathogenicity, which in turn validates ELMO1 as a potential RA therapeutic target. This study illustrated the power of MEG-based approaches for therapeutic target identification.

Indexed as

Adaptor Proteins, Signal TransducingArthritis, RheumatoidCell MovementCell ProliferationDNA MethylationFibroblastsGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksGenome-Wide Association StudyHumansProteomicsrac1 GTP-Binding ProteinRNA, Small InterferingSynovial MembraneAdaptor Proteins, Signal TransducingELMO1 protein, humanrac1 GTP-Binding ProteinRAC1 protein, humanRNA, Small Interfering

Identifiers

PMID25901943
PMCPMC4406750
OpenAlexW2078298511

What OpenQuestion holds

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LicenceCC BY
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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.