Evidence map›Paper›PMID 26363782›Full record

ArticleDiabetologia2015

A novel Dock8 gene mutation confers diabetogenic susceptibility in the LEW.1AR1/Ztm-iddm rat, an animal model of human type 1 diabetes.

Tanja Arndt, Dirk Wedekind, Anne Jörns, Georgios Tsiavaliaris, Edwin Cuppen, Hans-Jürgen Hedrich, Sigurd Lenzen

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Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

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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 2 institutions in 2 countries.

Tanja ArndtInstitute of Clinical Biochemistry, Hannover Medical School, 30623, Hannover, Germany.
Dirk WedekindInstitute for Laboratory Animal Science, Hannover Medical School, 30623, Hannover, Germany. wedekind.dirk@mh-hannover.de.
Anne JörnsInstitute of Clinical Biochemistry, Hannover Medical School, 30623, Hannover, Germany.
Georgios TsiavaliarisInstitute for Biophysical Chemistry, Hannover Medical School, Hannover, Germany.
Edwin CuppenCentre for Biomedical Genetics, Hubrecht Institute, Utrecht, The Netherlands.
Hans-Jürgen HedrichInstitute for Laboratory Animal Science, Hannover Medical School, 30623, Hannover, Germany.
Sigurd LenzenInstitute of Clinical Biochemistry, Hannover Medical School, 30623, Hannover, Germany. lenzen.sigurd@mh-hannover.de.
Medizinische Hochschule Hannover · DEHubrecht Institute for Developmental Biology and Stem Cell Research · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisThe LEW.1AR1-iddm rat, an animal model of human type 1 diabetes, arose through a spontaneous mutation within the inbred strain LEW.1AR1. A susceptibility locus (Iddm8) on rat chromosome 1 (RNO1) has been identified previously, which is accompanied by autoimmune diabetes and the additional phenotype of a variable CD3(+) T cell frequency.

methodsIn the present study we characterised the Iddm8 region on RNO1 in backcross strains using the genetically divergent Brown Norway (BN) and Paris (PAR) rats. Candidate genes of the Iddm8 region were sequenced for mutation analysis.

resultsThe Iddm8 region could be subdivided by single nucleotide polymorphism (SNP) analyses. In the first region, a mutation in exon 44 of the Dock8 gene was identified resulting in an amino acid exchange in the protein from glutamine to glutamate. This exchange is unique for the LEW.1AR1-iddm rat. In the second region, a SNP was detected in exon 11 of the Vwa2 gene with an exchange from arginine to tryptophan. This SNP is also present in other rat strains. CONCLUSIONS/

interpretationThe Dock8 mutation gave rise to a new type 1 diabetes rat model with very close similarity to type 1 diabetes in humans, providing a deepened insight into the impact of genes involved in diabetes development.

Indexed as

MutationAllelesAmino Acid SubstitutionAnimalsDiabetes Mellitus, Type 1Disease Models, AnimalDisease SusceptibilityExonsGuanine Nucleotide Exchange FactorsHumansKiller Cells, NaturalModels, MolecularPolymorphism, Single NucleotideRatsRats, Inbred LewReceptor-CD3 Complex, Antigen, T-CellDock8 protein, ratGuanine Nucleotide Exchange FactorsReceptor-CD3 Complex, Antigen, T-Cellvon Willebrand FactorAnimal modelMutationT cellsType 1 diabetes

Identifiers

PMID26363782
OpenAlexW1951469632

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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.