Evidence map›Paper›PMID 26912320›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Systematic Evaluation of Genes and Genetic Variants Associated with Type 1 Diabetes Susceptibility.

Ramesh Ram, Munish Mehta, Quang T Nguyen, Irma Larma, Bernhard O Boehm, Flemming Pociot, Patrick Concannon, Grant Morahan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 50 citations in OpenAlex.

  1. Gain-of-function mutation inbioRxiv : the preprint server for biology · 2026
    Article
  2. Type 1 Diabetes Genetics Consortium.The Journal of clinical endocrinology and metabolism · 2025
    Review
  3. A Genetic Test to Identify People at High Risk of Heart Failure.International journal of molecular sciences · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Extracellular Vesicles in Type 1 Diabetes: A Versatile Tool.Bioengineering (Basel, Switzerland) · 2022
    Review
  12. The Genetics of Diabetes: What We Can Learn fromInternational journal of molecular sciences · 2021
    Review
  13. Diabetes · 2021
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. The Genetic Contribution to Type 1 Diabetes.Current diabetes reports · 2019
    Review
  20. Review
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

8 authors at 4 institutions in 5 countries.

Ramesh RamCentre for Diabetes Research, Harry Perkins Institute of Medical Research, Nedlands, Western Australia 6009, Australia; Centre of Medical Research, University of Western Australia, Nedlands, Western Australia 6009, Australia;ORCID http://orcid.org/0000-0002-4827-4778
Munish MehtaCentre for Diabetes Research, Harry Perkins Institute of Medical Research, Nedlands, Western Australia 6009, Australia; Centre of Medical Research, University of Western Australia, Nedlands, Western Australia 6009, Australia;ORCID http://orcid.org/0000-0003-1955-6976
Quang T NguyenCentre for Diabetes Research, Harry Perkins Institute of Medical Research, Nedlands, Western Australia 6009, Australia; Centre of Medical Research, University of Western Australia, Nedlands, Western Australia 6009, Australia;
Irma LarmaCentre for Diabetes Research, Harry Perkins Institute of Medical Research, Nedlands, Western Australia 6009, Australia; Centre of Medical Research, University of Western Australia, Nedlands, Western Australia 6009, Australia;ORCID http://orcid.org/0000-0003-2177-0488
Bernhard O BoehmLee Kong Chian School of Medicine, Nanyang Technological University, Singapore 636921; Ulm University Medical Centre, Department of Internal Medicine I, Ulm University, 89081 Ulm, Germany;
Flemming PociotDepartment of Pediatrics, Herlev and Gentofte Hospital, 2730 Herlev, Denmark;ORCID http://orcid.org/0000-0003-3274-5448
Patrick ConcannonDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL 32610; and Genetics Institute, University of Florida, Gainesville, FL 32610.
Grant MorahanCentre for Diabetes Research, Harry Perkins Institute of Medical Research, Nedlands, Western Australia 6009, Australia; Centre of Medical Research, University of Western Australia, Nedlands, Western Australia 6009, Australia; grant.morahan@uwa.edu.au.ORCID http://orcid.org/0000-0002-8562-7325
The University of Western Australia · AUHerlev Hospital · DKNanyang Technological University · SGUniversity of Florida · US

Funding

Expression and proteomic characterization of risk loci in type 1 diabetesDP3DK085678 · NIDDK · UNIVERSITY OF VIRGINIA · PI RICH, STEPHEN S. · 2009 to 2009
$6.6M
NIDDK NIH HHS 1DP3DK085678NIDDK NIH HHS DP3 DK085678
6 · The paper itself

Abstract

Genome-wide association studies have found >60 loci that confer genetic susceptibility to type 1 diabetes (T1D). Many of these are defined only by anonymous single nucleotide polymorphisms: the underlying causative genes, as well as the molecular bases by which they mediate susceptibility, are not known. Identification of how these variants affect the complex mechanisms contributing to the loss of tolerance is a challenge. In this study, we performed systematic analyses to characterize these variants. First, all known genes in strong linkage disequilibrium (r(2) > 0.8) with the reported single nucleotide polymorphisms for each locus were tested for commonly occurring nonsynonymous variations. We found only a total of 22 candidate genes at 16 T1D loci with common nonsynonymous alleles. Next, we performed functional studies to examine the effect of non-HLA T1D risk alleles on regulating expression levels of genes in four different cell types: EBV-transformed B cell lines (resting and 6 h PMA stimulated) and purified CD4(+) and CD8(+) T cells. We mapped cis-acting expression quantitative trait loci and found 24 non-HLA loci that affected the expression of 31 transcripts significantly in at least one cell type. Additionally, we observed 25 loci that affected 38 transcripts in trans. In summary, our systems genetics analyses defined the effect of T1D risk alleles on levels of gene expression and provide novel insights into the complex genetics of T1D, suggesting that most of the T1D risk alleles mediate their effect by influencing expression of multiple nearby genes.

Indexed as

Genetic Predisposition to DiseaseGenetic VariationCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell Line, TransformedDiabetes Mellitus, Type 1Epistasis, GeneticGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksGenetic Association StudiesGenome-Wide Association StudyGenotypeHumansLeukocytes, MononuclearLinkage Disequilibrium

Identifiers

PMID26912320
PMCPMC4799766
OpenAlexW2287906200

What OpenQuestion holds

Textmetadata
LicenceTDM
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.