Evidence map›Paper›PMID 19995791›Full record

ArticleHuman molecular genetics2010

Upstream transcription factor 1 influences plasma lipid and metabolic traits in mice.

Sulin Wu, Rebecca Mar-Heyming, Eric Z Dugum, Nicholas A Kolaitis, Hongxiu Qi, Päivi Pajukanta, Lawrence W Castellani, Aldons J Lusis, Thomas A Drake

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
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  9. Congenic mice demonstrate the presence of QTLs conferring obesity and hypercholesterolemia on chromosome 1 in the TALLYHO mouse.Mammalian genome : official journal of the International Mammalian Genome Society · 2017
    Article
  10. Article
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  12. Significant association between upstream transcription factor 1 rs2516839 polymorphism and hepatocellular carcinoma risk: a case-control study.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  13. Article
  14. DNA methylation of the LY86 gene is associated with obesity, insulin resistance, and inflammation.Twin research and human genetics : the official journal of the International Society for Twin Studies · 2014
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  15. Article
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  18. Role of the USF1 transcription factor in diabetic kidney disease.American journal of physiology. Renal physiology · 2011
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  19. Article
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

9 authors at 1 institution in 1 country.

Sulin WuDepartment of Human Genetics, David Geffen School of Medicine at University of California, Los Angeles, CA 90095, USA.
Rebecca Mar-Heyming
Eric Z Dugum
Nicholas A Kolaitis
Hongxiu Qi
Päivi Pajukanta
Lawrence W Castellani
Aldons J Lusis
Thomas A Drake
University of California, Los Angeles · US

Funding

Systems genomics of metabolic syndrome traitsP01HL028481 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REUE, KAREN · 1985 to 2019
$50.2M
Training Grant in Genomic Analysis and InterpretationT32HG002536 · NHGRI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Valerie A Arboleda, Harold Pimentel · 2002 to 2026
$8.6M
Genomics of dyslipidemia in MexicansR01HL095056 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PAJUKANTA, PAIVI · 2009 to 2018
$5.9M
Gene expression networks for metabolic syndrome traits in miceR01DK072206 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DRAKE, THOMAS A · 2006 to 2010
$1.5M
Genetic susceptibility to Common Lipid Disorders in MexicoR01HL082762 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PAJUKANTA, PAIVI · 2006 to 2009
$1.4M
NHGRI NIH HHS T32 HG002536NHGRI NIH HHS T32 HG02536NHLBI NIH HHS HL082762NHLBI NIH HHS HL095056NHLBI NIH HHS HL28481NHLBI NIH HHS P01 HL028481NHLBI NIH HHS R01 HL082762NHLBI NIH HHS R01 HL095056NIDDK NIH HHS DK072260NIDDK NIH HHS R01 DK072206
6 · The paper itself

Abstract

Upstream transcription factor 1 (USF1) has been associated with familial combined hyperlipidemia, the metabolic syndrome, and related conditions, but the mechanisms involved are unknown. In this study, we report validation of Usf1 as a causal gene of cholesterol homeostasis, insulin sensitivity and body composition in mouse models using several complementary approaches and identify associated pathways and gene expression network modules. Over-expression of human USF1 in both transgenic mice and mice with transient liver-specific over-expression influenced metabolic trait phenotypes, including obesity, total cholesterol level, LDL/VLDL cholesterol and glucose/insulin ratio. Additional analyses of trait and hepatic gene expression data from an F2 population derived from C57BL/6J and C3H/HeJ strains in which there is a naturally occurring variation in Usf1 expression supported a causal role for Usf1 for relevant metabolic traits. Gene network and pathway analyses of the liver gene expression signatures in the F2 population and the hepatic over-expression model suggested the involvement of Usf1 in immune responses and metabolism, including an Igfbp2-centered module. In all three mouse model settings, notable sex specificity was observed, consistent with human studies showing differences in association with USF1 gene polymorphisms between sexes.

Indexed as

AnimalsCholesterolDisease Models, AnimalFemaleHumansHyperlipidemia, Familial CombinedLipidsLiverMaleMiceMice, Inbred C3HMice, Inbred C57BLMice, TransgenicUpstream Stimulatory FactorsCholesterolLipidsUpstream Stimulatory FactorsUSF1 protein, human

Identifiers

PMID19995791
PMCPMC2807368
OpenAlexW2147283296

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.