Evidence map›Paper›PMID 12975465›Full record

ArticleThe Journal of clinical investigation2003

HATs off to Hop: recruitment of a class I histone deacetylase incriminates a novel transcriptional pathway that opposes cardiac hypertrophy.

Yasuo Hamamori, Michael D Schneider

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. The role of sirtuins in cardiac disease.American journal of physiology. Heart and circulatory physiology · 2015
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Yasuo HamamoriCenter for Cardiovascular Development, Baylor College of Medicine, One Baylor Plaza, Room 506D, Houston, Texas 77030, USA.
Michael D Schneider
Baylor College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone acetylation, regulated by two antagonistic enzymes - histone acetyltransferases (HATs) and histone deacetylases (HDACs) - results in transcriptional changes and also plays a critical role in cardiac development and disease. A new study shows that overexpression of the atypical transcriptional corepressor homeodomain-only protein (Hop) causes cardiac hypertrophy via recruitment of a class I HDAC. In contrast to the body of work on transcriptional mechanisms that drive cardiac hypertrophy, including class II HDACs, this report elucidates a novel growth-suppressing transcriptional pathway in cardiac muscle that opposes hypertrophic growth.

Indexed as

Transcription, GeneticAcetyltransferasesAnimalsCardiomegalyEnzyme InhibitorsHistone AcetyltransferasesHistone DeacetylasesHomeodomain ProteinsMyocardiumRepressor ProteinsSaccharomyces cerevisiae ProteinsAcetyltransferasesEnzyme InhibitorsHistone AcetyltransferasesHistone DeacetylasesHomeodomain ProteinsRepressor ProteinsSaccharomyces cerevisiae ProteinsNon-programmatic

Identifiers

PMID12975465
PMCPMC193677
OpenAlexW1978632238

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.