Evidence map›Paper›PMID 18354499›Full record

ArticleThe EMBO journal2008

Liver-specific deletion of histone deacetylase 3 disrupts metabolic transcriptional networks.

Sarah K Knutson, Brenda J Chyla, Joseph M Amann, Srividya Bhaskara, Stacey S Huppert, Scott W Hiebert

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

162 citing papers in PubMed, 265 citations in OpenAlex.

  1. Review
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  4. Article
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  6. Transcriptional repression by HDAC3 mediates T cell exclusion fromProceedings of the National Academy of Sciences of the United States of America · 2024
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102 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Sarah K KnutsonDepartment of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Brenda J Chyla
Joseph M Amann
Srividya Bhaskara
Stacey S Huppert
Scott W Hiebert
Vanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
BIOCHEMICAL &CHEMICAL TRAINING FOR CANCER RESEARCHT32CA009582 · NCI · VANDERBILT UNIVERSITY · PI David K Cortez · 1987 to 2026
$8.8M
Role of AML1-ETO in Acute LeukemiaR01CA064140 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 1994 to 2018
$5.7M
VIRUSES, NUCLEIC ACIDS, GROWTH, AND CANCERT32CA009385 · NCI · VANDERBILT UNIVERSITY · PI RULEY, HENRY EARL · 1985 to 2007
$4.1M
TEL AND THE T(12--21) AND B CELL ALLR01CA077274 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 1997 to 2006
$2.1M
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NCI NIH HHS R01 CA064140NCI NIH HHS R01 CA077274NCI NIH HHS R01-CA64140NCI NIH HHS R01-CA77274NCI NIH HHS T32 CA009385NCI NIH HHS T32 CA009582NIDDK NIH HHS 5P30DK58404NIDDK NIH HHS P30 DK058404
6 · The paper itself

Abstract

Histone deacetylase 3 (Hdac3) is an enzymatic component of transcriptional repression complexes recruited by the nuclear hormone receptors. Inactivation of Hdac3 in cancer cell lines triggered apoptosis, and removal of Hdac3 in the germ line of mice caused embryonic lethality. Therefore, we deleted Hdac3 in the postnatal mouse liver. These mice developed hepatomegaly, which was the result of hepatocyte hypertrophy, and these morphological changes coincided with significant imbalances between carbohydrate and lipid metabolism. Loss of Hdac3 triggered changes in gene expression consistent with inactivation of repression mediated by nuclear hormone receptors. Loss of Hdac3 also increased the levels of Ppar gamma2, and treatment of these mice with a Ppar gamma antagonist partially reversed the lipid accumulation in the liver. In addition, gene expression analysis identified mammalian target of rapamycin signalling as being activated after deletion of Hdac3, and inhibition by rapamycin affected the accumulation of neutral lipids in Hdac3-null livers. Thus, Hdac3 regulates metabolism through multiple signalling pathways in the liver, and deletion of Hdac3 disrupts normal metabolic homeostasis.

Indexed as

Gene DeletionGene Regulatory NetworksAcetylationAnimalsAnimals, NewbornCholesterolEnzyme ActivationEnzyme InhibitorsGene Expression RegulationHepatocytesHistone Deacetylase 3Histone DeacetylasesHomeostasisHypertrophyHypoglycemiaInsulinCholesterolCre recombinaseEnzyme InhibitorsHistone Deacetylase 3Histone DeacetylasesInsulinIntegrasesmTOR protein, mousePPAR gammaProtein KinasesTOR Serine-Threonine Kinases

Identifiers

PMID18354499
PMCPMC2323257
OpenAlexW2149370967

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.