Evidence map›Paper›PMID 25520036›Full record

ArticleG3 (Bethesda, Md.)2014

Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains.

Dai-Lun Shin, Ashutosh K Pandey, Jesse Dylan Ziebarth, Megan K Mulligan, Robert W Williams, Robert Geffers, Bastian Hatesuer, Klaus Schughart, Esther Wilk

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in G3 (Bethesda, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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

9 authors at 3 institutions in 2 countries.

Dai-Lun ShinDepartment of Infection Genetics, Helmholtz Centre for Infection Research and University of Veterinary Medicine Hannover, Braunschweig, Germany.
Ashutosh K PandeyDepartment of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
Jesse Dylan ZiebarthDepartment of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
Megan K MulliganDepartment of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
Robert W WilliamsDepartment of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
Robert GeffersResearch Group Genome Analytics, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Bastian HatesuerDepartment of Infection Genetics, Helmholtz Centre for Infection Research and University of Veterinary Medicine Hannover, Braunschweig, Germany.
Klaus SchughartDepartment of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
Esther WilkDepartment of Infection Genetics, Helmholtz Centre for Infection Research and University of Veterinary Medicine Hannover, Braunschweig, Germany Esther.Wilk@helmholtz-hzi.de.
University of Tennessee Health Science Center · USHelmholtz Centre for Infection Research · DEUniversity of Veterinary Medicine Hannover, Foundation · DE

Funding

Systems Genetics of Alcohol Response and Stress Effects in CNSU01AA013499 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WILLIAMS, ROBERT W. · 2002 to 2016
$4.8M
NIAAA NIH HHS U01 AA013499
6 · The paper itself

Abstract

Current model DBA/2J (D2J) mice lack CD94 expression due to a deletion spanning the last coding exon of the Klrd1 gene that occurred in the mid- to late 1980s. In contrast, DBA/2JRj (D2Rj) mice, crosses derived from DBA/2J before 1984, and C57BL/6J (B6) mice lack the deletion and have normal CD94 expression. For example, BXD lines (BXD1-32) generated in the 1970s by crossing B6 and D2J do not segregate for the exonic deletion and have high expression, whereas BXD lines 33 and greater were generated after 1990 are segregating for the deletion and have highly variable Klrd1 expression. We performed quantitative trait locus analysis of Klrd1 expression by using BXD lines with different generation times and found that the expression difference in Klrd1 in the later BXD set is driven by a strong cis-acting expression quantitative trait locus. Although the Klrd1/CD94 locus is essential for mousepox resistance, the genetic variation among D2 substrains and the later set of BXD strains is not associated with susceptibility to the Influenza A virus PR8 strain. Substrains with nearly identical genetic backgrounds that are segregating functional variants such as the Klrd1 deletion are useful genetic tools to investigate biological function.

Indexed as

AnimalsFemaleMice, Inbred DBAMutationNK Cell Lectin-Like Receptor Subfamily DQuantitative Trait LociNK Cell Lectin-Like Receptor Subfamily DBXDDBA/2Klrd1

Identifiers

PMID25520036
PMCPMC4321031
OpenAlexW2129940568

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.