Evidence map›Paper›PMID 22783727›Full record

ArticleGene expression2012

Distribution of histone3 lysine 4 trimethylation at T3-responsive loci in the heart during reversible changes in gene expression.

Kumar Pandya, Takahide Kohro, Imari Mimura, Mika Kobayashi, Youichiro Wada, Tatsuhiko Kodama, Oliver Smithies

Open access · hybridAbstract read
In one paragraph

Article in Gene expression, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Molecular Regulation of Cardiomyocyte Maturation.Current cardiology reports · 2025
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  8. Review
  9. Article
  10. Review
  11. Epigenetics of the failing heart.Heart failure reviews · 2015
    Review
  12. Review
  13. Article
  14. Review
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 2 institutions in 2 countries.

Kumar PandyaDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7525, USA.
Takahide Kohro
Imari Mimura
Mika Kobayashi
Youichiro Wada
Tatsuhiko Kodama
Oliver Smithies
The University of Tokyo · JPUniversity of North Carolina at Chapel Hill · US

Funding

MODELS FOR STUDYING THE GENETICS OF HYPERTENSIONR01HL049277 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1992 to 2025
$17.5M
NHLBI NIH HHS HL49277NHLBI NIH HHS R01 HL049277
6 · The paper itself

Abstract

Expression in the adult heart of a number of cardiac genes, including the two genes comprising the cardiac myosin heavy chain locus (Myh), is controlled by thyroid hormone (T3) levels, but there is minimal information concerning the epigenetic status of the genes when their expressions change. We fed mice normal chow or a propyl thio uracil (PTU, an inhibitor of T3 production) diet for 6 weeks, or the PTU diet for 6 weeks followed by normal chow for a further 2 weeks. Heart ventricles from these groups were then used for ChIP-seq analyses with an antibody to H3K4me3, a well-documented epigenetic marker of gene activation. The resulting data show that, at the Myh7 locus, H3K4me3 modifications are induced primarily at 5' transcribed region in parallel with increased expression of beta myosin heavy chain (MHC). At the Myh6 locus, decreases in H3K4me3 modifications occurred at the promoter and 5' transcribed region. Extensive H3K4me3 modifications also occurred at the intergenic region between the two Myh genes, which extended into the 3' transcribed region of Myh7. The PTU-induced changes in H3K4me3 levels are, for the most part, reversible but are not invariably complete. We found full restoration of Myh6 gene expression upon PTU withdrawal; however, the H3K4me3 pattern was only partially restored at Myh6, suggesting that full reexpression of Myh6 does not require that the H3K4me3 modifications return fully to the untreated conditions. Together, our data show that the H3K4me3 modification is an epigenetic marker closely associated with changes in Myh gene expression.

Indexed as

Administration, OralAnimalsAntithyroid AgentsBinding SitesBiomarkersChromatin ImmunoprecipitationDNA, IntergenicEpigenesis, GeneticGene ExpressionGenetic LociHeart VentriclesHistonesMethylationMiceMyosin Heavy ChainsPropylthiouracilAntithyroid AgentsBiomarkersDNA, IntergenicHistonesMyh7 protein, mouseMyosin Heavy ChainsPropylthiouracilRegulatory Sequences, Ribonucleic AcidTriiodothyronine

Identifiers

PMID22783727
PMCPMC3607203
OpenAlexW2050822151

What OpenQuestion holds

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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.