Evidence map›Paper›PMID 23229551›Full record

ArticleThe Journal of biological chemistry2013

Transcriptional regulation patterns revealed by high resolution chromatin immunoprecipitation during cardiac hypertrophy.

Danish Sayed, Minzhen He, Zhi Yang, Lin Lin, Maha Abdellatif

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

38 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. BET Protein-Mediated Transcriptional Regulation in Heart Failure.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Epigenetic therapies in heart failure.Journal of molecular and cellular cardiology · 2019
    Article
  16. Article
  17. Article
  18. Disruption of cardiac Med1 inhibits RNA polymerase II promoter occupancy and promotes chromatin remodeling.American journal of physiology. Heart and circulatory physiology · 2019
    Article
  19. Article
  20. Epigenomes in Cardiovascular Disease.Circulation research · 2018
    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

5 authors at 1 institution in 1 country.

Danish SayedCardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, Newark, New Jersey 07103, USA.
Minzhen He
Zhi Yang
Lin Lin
Maha Abdellatif
Boston Children's Hospital · US

Funding

Mechanisms of RasGAP in cardiac cell growth and survivalR01HL057970 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ABDELLATIF, MAHA · 2004 to 2014
$2.8M
The role of microRNA in cardiac cell deathR01HL104115 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ABDELLATIF, MAHA · 2010 to 2014
$1.6M
Mechanisms in transcriptional regulation during cardiac hypertrophyR01HL119726 · NHLBI · RBHS-NEW JERSEY MEDICAL SCHOOL · PI ABDELLATIF, MAHA · 2013 to 2016
$1.6M
RAS DEPENDENT SIGNALING IN CARDIAC HYPERTROPHYR29HL057970 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ABDELLATIF, MAHA · 1998 to 2002
$297k
NHLBI NIH HHS HL057970NHLBI NIH HHS HL104115NHLBI NIH HHS R01 HL057970NHLBI NIH HHS R01 HL104115NHLBI NIH HHS R01 HL119726NHLBI NIH HHS R29 HL057970
6 · The paper itself

Abstract

Cardiac hypertrophy is characterized by a generalized increase in gene expression that is commensurate with the increase in myocyte size and mass, on which is superimposed more robust changes in the expression of specialized genes. Both transcriptional and posttranscriptional mechanisms play fundamental roles in these processes; however, genome-wide characterization of the transcriptional changes has not been investigated. Our goal was to identify the extent and modes, RNA polymerase II (pol II) pausing versus recruitment, of transcriptional regulation underlying cardiac hypertrophy. We used anti-pol II and anti-histone H3K9-acetyl (H3K9ac) chromatin immunoprecipitation-deep sequencing to determine the extent of pol II recruitment and pausing, and the underlying epigenetic modifications, respectively, during cardiac growth. The data uniquely reveal two mutually exclusive modes of transcriptional regulation. One involves an incremental increase (30-50%) in the elongational activity of preassembled, promoter-paused, pol II, and encompasses ∼25% of expressed genes that are essential/housekeeping genes (e.g. RNA synthesis and splicing). Another involves a more robust activation via de novo pol II recruitment, encompassing ∼5% of specialized genes (e.g. contractile and extracellular matrix). Moreover, the latter subset has relatively shorter 3'-UTRs with fewer predicted targeting miRNA, whereas most miRNA targets fall in the former category, underscoring the significance of posttranscriptional regulation by miRNA. The results, for the first time, demonstrate that promoter-paused pol II plays a role in incrementally increasing housekeeping genes, proportionate to the increase in heart size. Additionally, the data distinguish between the roles of posttranscriptional versus transcriptional regulation of specific genes.

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsAnimals, NewbornCardiomegalyChromatin ImmunoprecipitationGenome-Wide Association StudyHeartHistonesImmunoprecipitationMiceMice, Inbred C57BLMyocardiumPromoter Regions, GeneticRNA Polymerase IIHistonesRNA Polymerase II

Identifiers

PMID23229551
PMCPMC3554922
OpenAlexW1987261387

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.