Evidence map›Paper›PMID 26689548›Full record

ArticlePloS one2015

The Signal Transducer and Activator of Transcription 1 (STAT1) Inhibits Mitochondrial Biogenesis in Liver and Fatty Acid Oxidation in Adipocytes.

Jennifer D Sisler, Magdalena Morgan, Vidisha Raje, Rebecca C Grande, Marta Derecka, Jeremy Meier, Marc Cantwell, Karol Szczepanek, William J Korzun, Edward J Lesnefsky and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 47 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

13 authors at 4 institutions in 1 country.

Jennifer D SislerDepartment of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
Magdalena MorganDepartment of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
Vidisha RajeDepartment of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
Rebecca C GrandeDepartment of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA, 22908, United States of America.
Marta DereckaDepartment of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
Jeremy MeierDepartment of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
Marc CantwellDepartment of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
Karol SzczepanekDepartment of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
William J KorzunDepartment of Clinical Chemistry, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
Edward J LesnefskyDepartment of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
Thurl E HarrisDepartment of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA, 22908, United States of America.
Colleen M CronigerDepartment of Nutrition, Case Western University School of Medicine, Cleveland, OH, 44106, United States of America.
Andrew C LarnerDepartment of Biochemistry and Molecular Biology, and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, 23298, United States of America.
Virginia Commonwealth University · USUniversity of Virginia · USCase Western Reserve University · USHunter Holmes McGuire VA Medical Center · US

Funding

VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
Role of Oxidized neutral lipids in adipocyte functionR01DK101946 · NIDDK · UNIVERSITY OF VIRGINIA · PI HARRIS, THURL E. · 2014 to 2018
$1.7M
The Jak/Stat Pathway and Mitochondrial FunctionR01GM101677 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI LARNER, ANDREW CHARLES · 2012 to 2015
$1.1M
The Role of the tyrosine kinase Tyk2 in regulation of obesityR01DK099732 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LARNER, ANDREW CHARLES · 2014 to 2016
$919k
NIDDK NIH HHS 1R01 DK099732NIDDK NIH HHS R01 DK099732NIDDK NIH HHS R01 DK101946NIGMS NIH HHS 1R01GM101677-01A1NIGMS NIH HHS R01 GM101677NINDS NIH HHS 5P30NS047463NINDS NIH HHS P30 NS047463
6 · The paper itself

Abstract

The transcription factor STAT1 plays a central role in orchestrating responses to various pathogens by activating the transcription of nuclear-encoded genes that mediate the antiviral, the antigrowth, and immune surveillance effects of interferons and other cytokines. In addition to regulating gene expression, we report that STAT1-/- mice display increased energy expenditure and paradoxically decreased release of triglycerides from white adipose tissue (WAT). Liver mitochondria from STAT1-/- mice show both defects in coupling of the electron transport chain (ETC) and increased numbers of mitochondria. Consistent with elevated numbers of mitochondria, STAT1-/- mice expressed increased amounts of PGC1α, a master regulator of mitochondrial biogenesis. STAT1 binds to the PGC1α promoter in fed mice but not in fasted animals, suggesting that STAT1 inhibited transcription of PGC1α. Since STAT1-/- mice utilized more lipids we examined white adipose tissue (WAT) stores. Contrary to expectations, fasted STAT1-/- mice did not lose lipid from WAT. β-adrenergic stimulation of glycerol release from isolated STAT1-/- WAT was decreased, while activation of hormone sensitive lipase was not changed. These findings suggest that STAT1-/- adipose tissue does not release glycerol and that free fatty acids (FFA) re-esterify back to triglycerides, thus maintaining fat mass in fasted STAT1-/- mice.

Indexed as

AdipocytesAnimalsElectron Transport Chain Complex ProteinsFatty AcidsMiceMice, KnockoutMitochondria, LiverOxidation-ReductionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaResponse ElementsSTAT1 Transcription FactorTranscription FactorsTriglyceridesElectron Transport Chain Complex ProteinsFatty AcidsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseStat1 protein, mouseSTAT1 Transcription FactorTranscription FactorsTriglycerides

Identifiers

PMID26689548
PMCPMC4686975
OpenAlexW2200209017

What OpenQuestion holds

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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.