Evidence map›Paper›PMID 22498810›Full record

ArticleJournal of lipid research2012

Using bioinformatics and systems genetics to dissect HDL-cholesterol genetics in an MRL/MpJ x SM/J intercross.

Magalie S Leduc, Rachael Hageman Blair, Ricardo A Verdugo, Shirng-Wern Tsaih, Kenneth Walsh, Gary A Churchill, Beverly Paigen

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 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 4 institutions in 1 country.

Magalie S LeducThe Jackson Laboratory, Bar Harbor, ME, USA. mleduc@txbiomedgenetics.org
Rachael Hageman Blair
Ricardo A Verdugo
Shirng-Wern Tsaih
Kenneth Walsh
Gary A Churchill
Beverly Paigen
Jackson Laboratory · USMedical College of Wisconsin · USTexas Biomedical Research Institute · USUniversity at Buffalo, State University of New York · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI Mark D ADAMS · 1985 to 2026
$61.9M
Systems Genetic Analysis of Multi-parent CrossesR01GM070683 · NIGMS · JACKSON LABORATORY · PI BROMAN, KARL W, CHURCHILL, GARY A · 2004 to 2022
$6.8M
From QTL to Gene for HDL CholesterolR37HL077796 · NHLBI · JACKSON LABORATORY · PI PAIGEN, BEVERLY J · 2009 to 2018
$4.3M
Cloning QTL Genes for Plasma HDL CholesterolR01HL081162 · NHLBI · JACKSON LABORATORY · PI KORSTANJE, RONNY · 2006 to 2013
$3.3M
From QTL to Gene for HDL CholesterolR01HL077796 · NHLBI · JACKSON LABORATORY · PI PAIGEN, BEVERLY J · 2004 to 2008
$2.1M
Bayesian Dynamic Genome Scale Modeling of HDL Cholesterol TransportF32HL095240 · NHLBI · JACKSON LABORATORY · PI HAGEMAN, RACHAEL · 2009 to 2011
$135k
NCI NIH HHS CA034196NCI NIH HHS P30 CA034196NHLBI NIH HHS 1F32HL095240NHLBI NIH HHS F32 HL095240NHLBI NIH HHS HL-077796NHLBI NIH HHS HL-081162NHLBI NIH HHS R01 HL077796NHLBI NIH HHS R01 HL081162NHLBI NIH HHS R37 HL077796NIGMS NIH HHS GM-070683NIGMS NIH HHS R01 GM070683
6 · The paper itself

Abstract

A higher incidence of coronary artery disease is associated with a lower level of HDL-cholesterol. We searched for genetic loci influencing HDL-cholesterol in F2 mice from a cross between MRL/MpJ and SM/J mice. Quantitative trait loci (QTL) mapping revealed one significant HDL QTL (Apoa2 locus), four suggestive QTL on chromosomes 10, 11, 13, and 18 and four additional QTL on chromosomes 1 proximal, 3, 4, and 7 after adjusting HDL for the strong Apoa2 locus. A novel nonsynonymous polymorphism supports Lipg as the QTL gene for the chromosome 18 QTL, and a difference in Abca1 expression in liver tissue supports it as the QTL gene for the chromosome 4 QTL. Using weighted gene co-expression network analysis, we identified a module that after adjustment for Apoa2, correlated with HDL, was genetically determined by a QTL on chromosome 11, and overlapped with the HDL QTL. A combination of bioinformatics tools and systems genetics helped identify several candidate genes for both the chromosome 11 HDL and module QTL based on differential expression between the parental strains, cis regulation of expression, and causality modeling. We conclude that integrating systems genetics to a more-traditional genetics approach improves the power of complex trait gene identification.

Indexed as

Hybridization, GeneticAmino Acid SequenceAnimalsCholesterol, HDLChromosomes, MammalianDogsFemaleGenomicsHumansLipaseMaleMiceMolecular Sequence DataQuantitative Trait LociRatsSystems BiologyCholesterol, HDLLipaseLipg protein, mouse

Identifiers

PMID22498810
PMCPMC3351823
OpenAlexW2168548026

What Socratic 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 Socratic graph.