ArticleBMC genetics2016
Genetic dissection of the fatty liver QTL Fl1sa by using congenic mice and identification of candidate genes in the liver and epididymal fat.
Article in BMC genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Serotonin transporter-deficient mice display enhanced adipose tissue inflammation after chronic high-fat diet feeding.Frontiers in immunology · 2023Article
- Ablation of Iah1, a candidate gene for diet-induced fatty liver, does not affect liver lipid accumulation in mice.PloS one · 2020Article
- Gene regulation underlies environmental adaptation in house mice.Genome research · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
backgroundNonalcoholic fatty liver disease (NAFLD) is a multifactorial disease caused by interactions between environmental and genetic factors. The SMXA-5 mouse is a high-fat diet-induced fatty liver model established from SM/J and A/J strains. We have previously identified Fl1sa, a quantitative trait locus (QTL) for fatty liver on chromosome 12 (centromere-53.06 Mb) of SMXA-5 mice. However, the chromosomal region containing Fl1sa was too broad. The aim of this study was to narrow the Fl1sa region by genetic dissection using novel congenic mice and to identify candidate genes within the narrowed Fl1sa region.
resultsWe established two congenic strains, R2 and R3, from parental A/J-12
conclusionsIn this study, using congenic mice analysis, we narrowed the chromosomal region containing Fl1sa to two regions of mouse chromosome 12. We then identified 4 candidate genes in Fl1sa: Iah1 and Rrm2 from the liver and Zfp125 and Nrcam from epididymal fat.
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