Evidence map›Paper›PMID 17653278›Full record

ArticlePloS one2007

Large-scale in silico mapping of complex quantitative traits in inbred mice.

Pengyuan Liu, Haris Vikis, Yan Lu, Daolong Wang, Ming You

Abstract read
In one paragraph

Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Hybrid mouse diversity panel: a panel of inbred mouse strains suitable for analysis of complex genetic traits.Mammalian genome : official journal of the International Mammalian Genome Society · 2012
    Review
  7. Article
  8. Integrative assessment of chlorine-induced acute lung injury in mice.American journal of respiratory cell and molecular biology · 2012
    Article
  9. Article
  10. Article
  11. Haplotype association mapping of acute lung injury in mice implicates activin a receptor, type 1.American journal of respiratory and critical care medicine · 2011
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Assessing the prospects of genome-wide association studies performed in inbred mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2010
    Article
  19. Article
  20. 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

5 authors.

Pengyuan LiuDepartment of Surgery and the Alvin J. Siteman Cancer Center, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Haris Vikis
Yan Lu
Daolong Wang
Ming You

Funding

Identification of Pulmonary Lung Tumor Resistance 1 QTL CandidatesR01ES013340 · NIEHS · WASHINGTON UNIVERSITY · PI YOU, MING · 2004 to 2008
$1.8M
Positioning Cloning of Lung Cancer Modifier Gene Par2R01CA099147 · NCI · WASHINGTON UNIVERSITY · PI YOU, MING · 2003 to 2007
$1.7M
Genetic Basis of Lung Tumor Progression in MiceR01CA099187 · NCI · WASHINGTON UNIVERSITY · PI YOU, MING · 2003 to 2006
$1.2M
Positional Cloning of the Pas 1 QTL in miceR01ES012063 · NIEHS · WASHINGTON UNIVERSITY · PI YOU, MING · 2003 to 2006
$1.2M
NCI NIH HHS CA099147NCI NIH HHS CA099187NCI NIH HHS R01 CA099147NCI NIH HHS R01 CA099187NIEHS NIH HHS ES012063NIEHS NIH HHS ES013340NIEHS NIH HHS R01 ES012063NIEHS NIH HHS R01 ES013340Wellcome Trust
6 · The paper itself

Abstract

Understanding the genetic basis of common disease and disease-related quantitative traits will aid in the development of diagnostics and therapeutics. The processs of gene discovery can be sped up by rapid and effective integration of well-defined mouse genome and phenome data resources. We describe here an in silico gene-discovery strategy through genome-wide association (GWA) scans in inbred mice with a wide range of genetic variation. We identified 937 quantitative trait loci (QTLs) from a survey of 173 mouse phenotypes, which include models of human disease (atherosclerosis, cardiovascular disease, cancer and obesity) as well as behavioral, hematological, immunological, metabolic, and neurological traits. 67% of QTLs were refined into genomic regions <0.5 Mb with approximately 40-fold increase in mapping precision as compared with classical linkage analysis. This makes for more efficient identification of the genes that underlie disease. We have identified two QTL genes, Adam12 and Cdh2, as causal genetic variants for atherogenic diet-induced obesity. Our findings demonstrate that GWA analysis in mice has the potential to resolve multiple tightly linked QTLs and achieve single-gene resolution. These high-resolution QTL data can serve as a primary resource for positional cloning and gene identification in the research community.

Indexed as

Disease Models, AnimalGenetic VariationADAM12 ProteinADAM ProteinsAnimalsAtherosclerosisCardiovascular DiseasesChromosome MappingGenetic Association StudiesGenetic LinkageGenome-Wide Association StudyHumansMembrane ProteinsMiceMice, Inbred StrainsModels, GeneticADAM12 ProteinADAM12 protein, humanAdam12 protein, mouseADAM ProteinsMembrane Proteins

Identifiers

PMID17653278
PMCPMC1920557

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.