Evidence map›Paper›PMID 29491471›Full record

ArticleEuropean journal of human genetics : EJHG2018

Molecular-genetic characterization of common, noncoding UBASH3A variants associated with type 1 diabetes.

Yan Ge, Patrick Concannon

Open access · bronzeAbstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. New Perspectives in Studying Type 1 Diabetes Susceptibility Biomarkers.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. TULA Proteins in Men, Mice, Hens, and Lice: Welcome to the Family.International journal of molecular sciences · 2023
    Review
  10. UBASH3A Interacts with PTPN22 to RegulateInternational journal of molecular sciences · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. De-coding genetic risk variants in type 1 diabetes.Immunology and cell biology · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. UBASH3A Regulates the Synthesis and Dynamics of TCR-CD3 Complexes.Journal of immunology (Baltimore, Md. : 1950) · 2019
    Article
  19. Review
  20. Evidence that UBASH3 is a causal gene for type 1 diabetes.European journal of human genetics : EJHG · 2018
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Yan GeDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, USA.ORCID http://orcid.org/0000-0003-2129-9438
Patrick ConcannonDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, USA. patcon@ufl.edu.
University 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
Novel T1D risk variants from genomic analyses in high risk familiesR01DK106718 · NIDDK · UNIVERSITY OF FLORIDA · PI CONCANNON, PATRICK · 2015 to 2018
$1.4M
NIDDK NIH HHS DP3 DK085678NIDDK NIH HHS R01 DK106718
6 · The paper itself

Abstract

Genome-wide association and fine-mapping studies have identified over 40 susceptibility regions for type 1 diabetes (T1D), a common autoimmune disease; however, most of the disease-associated variants are noncoding, and it remains a challenge to understand their biological contributions to T1D pathogenesis. One identified T1D risk locus is located at chromosome 21q22.3 where the most likely candidate gene is UBASH3A, a negative regulator of NF-κB signaling. Various noncoding variants in UBASH3A have been shown to be associated with T1D or other autoimmune diseases. Here we investigated four such SNPs-rs11203202, rs80054410, rs11203203, and rs1893592. We discovered a novel role for rs1893592 in T1D and showed that its minor allele protects against T1D. Our haplotype analysis identified three T1D-associated UBASH3A haplotypes, and revealed that risk for T1D is affected by additive effects of these four UBASH3A variants. In human primary CD4

Indexed as

Genetic Predisposition to DiseaseAdaptor Proteins, Signal TransducingAllelesCD4-Positive T-LymphocytesDiabetes Mellitus, Type 1FemaleGenome-Wide Association StudyHaplotypesHumansInterleukin-2MalePedigreePolymorphism, Single NucleotideSignal TransductionAdaptor Proteins, Signal TransducingInterleukin-2UBASH3A protein, human

Identifiers

PMID29491471
PMCPMC6018660
OpenAlexW2792387337

What OpenQuestion holds

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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.