Evidence map›Paper›PMID 27210752›Full record

ArticleCell reports2016

Striking Immune Phenotypes in Gene-Targeted Mice Are Driven by a Copy-Number Variant Originating from a Commercially Available C57BL/6 Strain.

Vinay S Mahajan, Ezana Demissie, Hamid Mattoo, Vinay Viswanadham, Ajit Varki, Robert Morris, Shiv Pillai

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

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 90 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 1 country.

Vinay S MahajanRagon Institute of MGH, MIT and Harvard, 400 Technology Square, Cambridge, MA 02139, USA.
Ezana DemissieRagon Institute of MGH, MIT and Harvard, 400 Technology Square, Cambridge, MA 02139, USA.
Hamid MattooRagon Institute of MGH, MIT and Harvard, 400 Technology Square, Cambridge, MA 02139, USA.
Vinay ViswanadhamRagon Institute of MGH, MIT and Harvard, 400 Technology Square, Cambridge, MA 02139, USA.
Ajit VarkiDepartments of Medicine and Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Robert MorrisRagon Institute of MGH, MIT and Harvard, 400 Technology Square, Cambridge, MA 02139, USA.
Shiv PillaiRagon Institute of MGH, MIT and Harvard, 400 Technology Square, Cambridge, MA 02139, USA. Electronic address: pillai@helix.mgh.harvard.edu.
Ragon Institute of MGH, MIT and Harvard · USUniversity of California, San Diego · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
Siglec Modulation of Inflammatory ResponsesP01HL107150 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LE, DZUNG T · 2011 to 2017
$18.0M
The importance of the IgG4 glycome in IgG4-related disease(s)U19AI110495 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI SHIV Subramaniam PILLAI · 2014 to 2026
$7.9M
BIOSYNTHESIS AND REGULATION OF SUBSTITUTED SIALIC ACIDSR01GM032373 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI VARKI, AJIT P · 1985 to 2022
$6.9M
Studies on Peripheral B Lymphocyte DevelopmentR01AI064930 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI PILLAI, SHIV SUBRAMANIAM · 2006 to 2016
$3.9M
BIOLOGY OF SIALIC ACIDS AND THEIR SUBSTITUTIONSR37GM032373 · NIGMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI VARKI, AJIT P · 1995 to 2004
$1.8M
NHLBI NIH HHS P01 HL107150NIAID NIH HHS R01 AI064930NIAID NIH HHS U19 AI110495NIDDK NIH HHS P30 DK043351NIGMS NIH HHS R01 GM032373NIGMS NIH HHS R37 GM032373
6 · The paper itself

Abstract

We describe a homozygous copy-number variant that disrupts the function of Dock2 in a commercially available C57BL/6 mouse strain that is widely used for backcrossing. This Dock2 allele was presumed to have spontaneously arisen in a colony of Irf5 knockout mice. We discovered that this allele has actually been inadvertently backcrossed into multiple mutant mouse lines, including two engineered to be deficient in Siae and Cmah. This particular commercially obtained subline of C57BL/6 mice also exhibits several striking immune phenotypes that have been previously described in the context of Dock2 deficiency. Inadvertent backcrossing of a number of gene-targeted mice into this background has complicated the interpretation of several immunological studies. In light of these findings, published studies involving immune or hematopoietic phenotypes in which these C57BL/6 mice have been used as controls, as experimental animals, or for backcrossing will need to be reinterpreted.

Indexed as

Gene TargetingAllelesAnimalsBase SequenceB-LymphocytesCD8-Positive T-LymphocytesChromosome SegregationChromosomes, MammalianCrosses, GeneticDNA Copy Number VariationsExonsFemaleGene DuplicationGenetic LociGenetic MarkersGTPase-Activating ProteinsDOCK2 protein, mouseGenetic MarkersGTPase-Activating ProteinsGuanine Nucleotide Exchange Factors

Identifiers

PMID27210752
PMCPMC4892502
OpenAlexW2398472827

What OpenQuestion holds

Textmetadata
LicenceTDM
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.