Evidence map›Paper›PMID 18772481›Full record

ArticleJournal of lipid research2009

Genetic basis of HDL variation in 129/SvImJ and C57BL/6J mice: importance of testing candidate genes in targeted mutant mice.

Zhiguang Su, Xiaosong Wang, Shirng-Wern Tsaih, Aihong Zhang, Allison Cox, Susan Sheehan, Beverly Paigen

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Influence of allelic differences in Down syndrome.Progress in brain research · 2020
    Review
  4. Deletion of Nrip1 Extends Female Mice Longevity, Increases Autophagy, and Delays Cell Senescence.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018
    Article
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  14. Identification of novel mouse genes conferring posthypoxic pauses.Journal of applied physiology (Bethesda, Md. : 1985) · 2012
    Article
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  17. Review
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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 1 institution in 1 country.

Zhiguang SuThe Jackson Laboratory, Bar Harbor, ME 04609, USA.
Xiaosong Wang
Shirng-Wern Tsaih
Aihong Zhang
Allison Cox
Susan Sheehan
Beverly Paigen
Jackson Laboratory · US

Funding

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
Identifying Genes Regulating HDL Cholesterol LevelsR01HL074086 · NHLBI · JACKSON LABORATORY · PI PAIGEN, BEVERLY J · 2004 to 2007
$994k
NHLBI NIH HHS HL74086NHLBI NIH HHS HL77796NHLBI NIH HHS HL 81162NHLBI NIH HHS R01 HL074086NHLBI NIH HHS R01 HL077796NHLBI NIH HHS R01 HL081162NHLBI NIH HHS R37 HL077796
6 · The paper itself

Abstract

To evaluate the effect of genetic background on high-density lipoprotein cholesterol (HDL) levels in Soat1(-/-) mice, we backcrossed sterol O-acyltransferase 1 (Soat1)(-/-) mice, originally reported to have elevated HDL levels, to C57BL/6 mice and constructed a congenic strain with only a small region (3.3Mb) of 129 alleles, specifically excluding the nearby apolipoprotein A-II (Apoa2) gene from 129. HDL levels in these Soat1(-/-) mice were no different from C57BL/6, indicating that the passenger gene Apoa2 caused the previously reported elevation of HDL in these Soat1(-/-) mice. Because many knockouts are made in strain 129 and then subsequently backcrossed into C57BL/6, it is important to identify quantitative trait loci (QTL) that differ between 129 and C57BL/6 so that one can guard against effects ascribed to a knockout but really caused by a passenger gene from 129. To provide such data, we generated 528 F(2) progeny from an intercross of 129S1/SvImJ and C57BL/6 and measured HDL concentrations in F(2) animals first fed chow and then atherogenic diet. A genome wide scan using 508 single-nucleotide polymorphisms (SNPs) identified 19 QTL, 2 of which were male specific and 2 were female specific. Using comparative genomics and haplotype analysis, we narrowed QTL on chromosomes 3, 5, 8, 17, and 18 to 0.5, 6.3, 2.6, 1.1, and 0.6 Mb, respectively. These data will serve as a reference for any effort to test the impact of candidate genes on HDL using a knockout strategy.

Indexed as

MutationAnimalsCrosses, GeneticDiet, AtherogenicFemaleGenetic VariationGenomeGenotypeHaplotypesLipoproteins, HDLMaleMiceMice, Inbred C57BLMice, KnockoutQuantitative Trait LociLipoproteins, HDL

Identifiers

PMID18772481
PMCPMC2602865
OpenAlexW2105282353

What OpenQuestion 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 OpenQuestion graph.