Evidence map›Paper›PMID 19956107›Full record

SynthesisGenes and immunity2009

Follow-up of 1715 SNPs from the Wellcome Trust Case Control Consortium genome-wide association study in type I diabetes families.

J D Cooper, N M Walker, D J Smyth, K Downes, B C Healy, J A Todd, Type I Diabetes Genetics Consortium

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Genes and immunity, 2009. 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
3.8field-weighted citation impact, top 6% 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, 59 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Mechanisms underlying sex differences in autoimmunity.The Journal of clinical investigation · 2024
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Influence ofFrontiers in immunology · 2021
    Review
  9. Article
  10. Type 1 diabetes: genes associated with disease development.Central-European journal of immunology · 2020
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Molecular mechanisms in autoimmune type 1 diabetes: a critical review.Clinical reviews in allergy & immunology · 2014
    Review
  17. Review
  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

7 authors at 4 institutions in 1 country.

J D CooperJuvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge, UK. Jason.Cooper@cimr.cam.ac.uk
N M Walker
D J Smyth
K Downes
B C Healy
J A Todd
Type I Diabetes Genetics Consortium
Addenbrooke's Hospital · GBUniversity of Cambridge · GBJuvenile Diabetes Research Foundation · GBWellcome Trust · GB

Funding

Type 1 Diabetes Genetics ConsortiumU01DK062418 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RICH, STEPHEN S. · 2002 to 2007
$59.8M
AN NCRR CENTER FOR HIGH THROUGHPUT SNP GENOTYPING AND ANALYSIS: GAIN NETWORKU54RR020278 · NCRR · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GABRIEL, STACEY · 2004 to 2008
$14.4M
NCRR NIH HHS U54 RR020278NIDDK NIH HHS U01 DK062418Wellcome Trust 061858Wellcome Trust 079895
6 · The paper itself

Abstract

The advent of genome-wide association (GWA) studies has revolutionized the detection of disease loci and provided abundant evidence for previously undetected disease loci that can be pooled together in meta-analysis studies or used to design follow-up studies. A total of 1715 SNPs from the Wellcome Trust Case Control Consortium GWA study of type I diabetes (T1D) were selected and a follow-up study was conducted in 1410 affected sib-pair families assembled by the Type I Diabetes Genetics Consortium. In addition to the support for previously identified loci (PTPN22/1p13; ERBB3/12q13; SH2B3/12q24; CLEC16A/16p13; UBASH3A/21q22), evidence supporting two new and distinct chromosome locations associated with T1D was observed: FHOD3/18q12 (rs2644261, P=5.9 x 10(-4)) and Xp22 (rs5979785, P=6.8 x 10(-3); http://www.T1DBase.org). There was independent support for both SNPs in a GWA meta-analysis of 7514 cases and 9045 controls (P values=5.0 x 10(-3) and 6.7 x 10(-6), respectively). The chromosome 18q12 region contains four genes, none of which are obvious functional candidate genes. In contrast, the Xp22 SNP is located 30 kb centromeric of the functional candidate genes TLR8 and TLR7 genes. Both TLR8 and TLR7 are functional candidate genes owing to their key roles as pathogen recognition receptors and, in the case of TLR7, overexpression has been associated directly with murine autoimmune disease.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyPolymorphism, Single NucleotideAnimalsCase-Control StudiesDiabetes Mellitus, Type 1FemaleFollow-Up StudiesHumansLupus Erythematosus, SystemicMaleMiceNuclear Family

Identifiers

PMID19956107
PMCPMC2805462
OpenAlexW2018249504

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.