Evidence map›Paper›PMID 32694640›Full record

ArticleScientific reports2020

UBASH3A deficiency accelerates type 1 diabetes development and enhances salivary gland inflammation in NOD mice.

Yi-Guang Chen, Ashley E Ciecko, Shamim Khaja, Michael Grzybowski, Aron M Geurts, Scott M Lieberman

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. STS2 deficiency revives CD8Journal for immunotherapy of cancer · 2025
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. UBASH3A Interacts with PTPN22 to RegulateInternational journal of molecular sciences · 2023
    Article
  11. Genetic and Molecular Quality Control of Genetically Engineered Mice.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. De-coding genetic risk variants in type 1 diabetes.Immunology and cell biology · 2021
    Review
  16. 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

6 authors at 2 institutions in 1 country.

Yi-Guang ChenDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, 53226, USA. yichen@mcw.edu.
Ashley E CieckoDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI, 53226, USA.
Shamim KhajaDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, 53226, USA.
Michael GrzybowskiDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI, 53226, USA.
Aron M GeurtsDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI, 53226, USA.
Scott M LiebermanStead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, IA, 52242, USA.
Medical College of Wisconsin · USUniversity of Iowa · US

Funding

Mechanistic and Therapeutic Role of the CD137-CD137L Axis in Type 1 DiabetesR01DK107541 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG, RIDGWAY, WILLIAM M · 2016 to 2025
$5.6M
Discovery and Functional Studies of Genes for T1D GWAS Susceptibility LociDP3DK097605 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG, GEURTS, ARON M · 2012 to 2012
$4.3M
Cytokines driving T cell dysregulation in lacrimal gland autoimmunityR01EY027731 · NEI · UNIVERSITY OF IOWA · PI LIEBERMAN, SCOTT MATTHEW · 2018 to 2022
$2.4M
Shaping diabetogenic T cells by IL-27 in type 1 diabetesR01DK121747 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG · 2019 to 2022
$1.5M
Genetic analysis of islet-infiltrating IL-21-expressing CD4 T cells in type 1 diabetesR21AI144360 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG · 2020 to 2021
$418k
NEI NIH HHS R01 EY027731NIAID NIH HHS R21 AI144360NIDDK NIH HHS DP3 DK097605NIDDK NIH HHS R01 DK107541NIDDK NIH HHS R01 DK121747NIH HHS DK097605NIH HHS EY027731
6 · The paper itself

Abstract

Recent advances in genetic analyses have significantly refined human type 1 diabetes (T1D) associated loci. The goal of such effort is to identify the causal genes and have a complete understanding of the molecular pathways that independently or interactively influence cellular processes leading to the destruction of insulin producing pancreatic β cells. UBASH3A has been suggested as the underlying gene for a human T1D associated region on chromosome 21. To further evaluate the role of UBASH3A in T1D, we targeted Ubash3a in NOD mice using zinc-finger nuclease mediated mutagenesis. In both 10-week-old females and males, significantly more advanced insulitis was observed in UBASH3A-deficient than in wild-type NOD mice. Consistently, UBASH3A-deficient NOD mice developed accelerated T1D in both sexes, which was associated with increased accumulation of β-cell autoreactive T cells in the spleen and pancreatic lymph node. Adoptive transfer of splenic T cells into NOD.Rag1

Indexed as

Adoptive TransferAnimalsAutoimmunityCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesDiabetes Mellitus, Type 1Disease Models, AnimalFemaleGenetic Predisposition to DiseaseInsulin-Secreting CellsMaleMiceMice, Inbred NODMice, KnockoutMutagenesisReceptors, Antigen, T-CellReceptors, Antigen, T-CellSts-2 protein, mouseZinc Finger Nucleases

Identifiers

PMID32694640
PMCPMC7374577
OpenAlexW3043828248

What OpenQuestion holds

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LicenceCC BY
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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.