Evidence map›Paper›PMID 23007391›Full record

ArticleThe Journal of biological chemistry2012

Acetylation of myocardin is required for the activation of cardiac and smooth muscle genes.

Dongsun Cao, Chunbo Wang, Ruhang Tang, Huaqun Chen, Zheng Zhang, Mariko Tatsuguchi, Da-Zhi Wang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 37 citations in OpenAlex.

  1. Spatial expression of myocardin protein in normal and disease states.American journal of physiology. Cell physiology · 2026
    Article
  2. Review
  3. Article
  4. SENP2 Promotes VSMC Phenotypic Switching via Myocardin De-SUMOylation.International journal of molecular sciences · 2022
    Article
  5. Review
  6. MRTF: Basic Biology and Role in Kidney Disease.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. DNA Methylation and Histone Modification in Hypertension.International journal of molecular sciences · 2018
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Myocardin in biology and disease.Journal of biomedical research · 2015
    Review
  16. Review
  17. Article
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 4 institutions in 2 countries.

Dongsun CaoDepartment of Cardiology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA.
Chunbo Wang
Ruhang Tang
Huaqun Chen
Zheng Zhang
Mariko Tatsuguchi
Da-Zhi Wang
Harvard University · USUniversity of North Carolina at Chapel Hill · USBoston Children's Hospital · USNanjing Normal University · CN

Funding

MicroRNAs, cardiac development and functionR01HL085635 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, DA-ZHI · 2007 to 2015
$3.2M
Transcriptional control of cardiac developmentR01HL075251 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, DA-ZHI · 2004 to 2007
$1.1M
NHLBI NIH HHS HL075251NHLBI NIH HHS HL085635NHLBI NIH HHS R01 HL075251NHLBI NIH HHS R01 HL085635
6 · The paper itself

Abstract

Myocardin belongs to the SAF-A/B, Acinus, PIAS (SAP) domain family of transcription factors and is specifically expressed in cardiac and smooth muscle. Myocardin functions as a transcriptional coactivator of SRF and is sufficient and necessary for smooth muscle gene expression. We have previously found that myocardin induces the acetylation of nucleosomal histones surrounding SRF-binding sites in the control regions of cardiac and smooth muscle genes through recruiting chromatin-modifying enzyme p300, yet no studies have determined whether myocardin itself is similarly modified. In this study, we show that myocardin is a direct target for p300-mediated acetylation. p300 acetylates lysine residues at the N terminus of the myocardin protein. Interestingly, a direct interaction between p300 and myocardin, which is mediated by the C terminus of myocardin, is required for the acetylation event. Acetylation of myocardin by p300 enhances the association of myocardin and SRF as well as the formation of the myocardin-SRF-CArG box ternary complex. Conversely, acetylation of myocardin decreases the binding of histone deacetylase 5 (HDAC5) to myocardin. Acetylation of myocardin is required for myocardin to activate smooth muscle genes. Our study demonstrates that acetylation plays a key role in modulating myocardin function in controlling cardiac and smooth muscle gene expression.

Indexed as

AcetylationAnimalsChromatinCOS CellsGene Expression ProfilingGene Expression RegulationHistonesMiceModels, BiologicalMuscle, SmoothMyocardinMyocardiumNuclear Proteinsp300-CBP Transcription FactorsSerum Response FactorSignal TransductionChromatinHistonesMyocardinNuclear Proteinsp300-CBP Transcription FactorsSerum Response FactorTrans-Activators

Identifiers

PMID23007391
PMCPMC3493894
OpenAlexW1976421909

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.