Evidence map›Paper›PMID 27207523›Full record

ArticleDiabetes2016

CRISPR-Cas9-Mediated Modification of the NOD Mouse Genome With Ptpn22R619W Mutation Increases Autoimmune Diabetes.

Xiaotian Lin, Stephane Pelletier, Sebastien Gingras, Stephanie Rigaud, Christian J Maine, Kristi Marquardt, Yang D Dai, Karsten Sauer, Alberto R Rodriguez, Greg Martin and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.8field-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

34 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. An autoimmunity-associated allele ofProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. An Autoimmunity-associated allele ofbioRxiv : the preprint server for biology · 2025
    Article
  6. Review
  7. Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Applications of Genome-Editing Technologies for Type 1 Diabetes.International journal of molecular sciences · 2023
    Review
  13. UBASH3A Interacts with PTPN22 to RegulateInternational journal of molecular sciences · 2023
    Article
  14. Review
  15. eLife · 2023
    Article
  16. Gene Editing and Human iPSCs in Cardiovascular and Metabolic Diseases.Advances in experimental medicine and biology · 2023
    Article
  17. Gene Editing in Mouse Zygotes Using the CRISPR/Cas9 System.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  18. Genetic Polymorphism ofMedicina (Kaunas, Lithuania) · 2022
    Review
  19. Article
  20. Proautoimmune Allele of Tyrosine Phosphatase, PTPN22, Enhances Tumor Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2021
    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

15 authors at 4 institutions in 1 country.

Xiaotian LinDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA.
Stephane PelletierDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN.
Sebastien GingrasDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Stephanie RigaudDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA.
Christian J MaineDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA.
Kristi MarquardtDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA.
Yang D DaiDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA.
Karsten SauerDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA.
Alberto R RodriguezMurine Genetics Core, The Scripps Research Institute, La Jolla, CA.
Greg MartinMurine Genetics Core, The Scripps Research Institute, La Jolla, CA.
Sergey KupriyanovMurine Genetics Core, The Scripps Research Institute, La Jolla, CA.
Ling JiangBarbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO.
Liping YuBarbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO.
Douglas R GreenDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN.
Linda A ShermanDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA lsherman@scripps.edu.
Scripps Research Institute · USSt. Jude Children's Research Hospital · USUniversity of Colorado Denver · USUniversity of Pittsburgh · US

Funding

PATHOGENESIS AND IMMUNOLOGY OF DISEASET32AI007244 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 1985 to 2022
$8.8M
PTPN22 R619W in NOD miceR56AI121145 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI SHERMAN, LINDA A · 2016 to 2016
$739k
Mutant PTPN22 in autoimmune miceR21AI119353 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI SHERMAN, LINDA A · 2015 to 2016
$523k
NIAID NIH HHS R21 AI119353NIAID NIH HHS R56 AI121145NIAID NIH HHS T32 AI007244
6 · The paper itself

Abstract

An allelic variant of protein tyrosine phosphatase nonreceptor type 22 (PTPN22), PTPN22(R620W), is strongly associated with type 1 diabetes (T1D) in humans and increases the risk of T1D by two- to fourfold. The NOD mouse is a spontaneous T1D model that shares with humans many genetic pathways contributing to T1D. We hypothesized that the introduction of the murine orthologous Ptpn22(R619W) mutation to the NOD genome would enhance the spontaneous development of T1D. We microinjected CRISPR-Cas9 and a homology-directed repair template into NOD single-cell zygotes to introduce the Ptpn22(R619W) mutation to its endogenous locus. The resulting Ptpn22(R619W) mice showed increased insulin autoantibodies and earlier onset and higher penetrance of T1D. This is the first report demonstrating enhanced T1D in a mouse modeling human PTPN22(R620W) and the utility of CRISPR-Cas9 for direct genetic alternation of NOD mice.

Indexed as

MutationAllelesAnimalsBlotting, WesternCRISPR-Cas SystemsDiabetes Mellitus, Type 1FemaleGenetic Predisposition to DiseaseGenomeGenotypeHumansMaleMiceMice, Inbred NODMice, KnockoutPolymorphism, Single NucleotideProtein Tyrosine Phosphatase, Non-Receptor Type 22Ptpn22 protein, mouse

Identifiers

PMID27207523
PMCPMC4955979
OpenAlexW2344515831

What OpenQuestion holds

Textmetadata
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.