Evidence map›Paper›PMID 11285237›Full record

ArticleThe EMBO journal2001

A role for histone deacetylase HDAC1 in modulating the transcriptional activity of MyoD: inhibition of the myogenic program.

A Mal, M Sturniolo, R L Schiltz, M K Ghosh, M L Harter

Abstract read
In one paragraph

Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

128 citing papers in PubMed, 252 citations in OpenAlex.

  1. Article
  2. Review
  3. [Potential Mechanisms and Research Advances of HDAC1 in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. The role of inner nuclear membrane protein emerin in myogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Emerging role of HDAC11 in skeletal muscle biology.Frontiers in cell and developmental biology · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Regulation of muscle stem cell fate.Cell regeneration (London, England) · 2022
    Review
  20. Article

68 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

5 authors at 1 institution in 1 country.

A MalDepartment of Molecular Biology, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
M Sturniolo
R L Schiltz
M K Ghosh
M L Harter
Cleveland Clinic · US

Funding

ROLE OF E1A IN INDUCING CELLULAR DNA SYNTHESISR01GM054014 · NIGMS · CLEVELAND CLINIC FOUNDATION · PI HARTER, NIKKI L · 1996 to 1999
–
NIGMS NIH HHS GM54014
6 · The paper itself

Abstract

The molecular mechanism(s) that are responsible for suppressing MyoD's transcriptional activities in undifferentiated skeletal muscle cells have not yet been determined. We now show that MyoD associates with a histone deacetylase-1 (HDAC1) in these cells and that this interaction is responsible for silencing MyoD-dependent transcription of endogenous p21 as well as muscle-specific genes. Specifically, we present evidence that HDAC1 can bind directly to MyoD and use an acetylated MyoD as a substrate in vitro, whereas a mutant version of HDAC1 (H141A) can not. Further more, this mutant also fails to repress MyoD-mediated transcription in vivo, and unlike wild-type HDAC1 it can not inhibit myogenic conversion, as judged by confocal microscopy. Finally, we show that an endogenous MyoD can be acetylated upon its conversion to a hypophosphorylated state and only when the cells have been induced to differentiate. These results provide for a model which postulates that MyoD may be co-dependent on HDAC1 and P/CAF for temporally controlling its transcriptional activity before and after the differentiation of muscle cells.

Indexed as

Transcription, GeneticAcetylationAcetyltransferasesAnimalsCell Cycle ProteinsCell DifferentiationCell LineCell Line, TransformedCyclin-Dependent Kinase Inhibitor p21CyclinsHistone AcetyltransferasesHistone Deacetylase 1Histone DeacetylasesHumansJurkat CellsMiceAcetyltransferasesCDKN1A protein, humanCdkn1a protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21CyclinsHDAC1 protein, humanHistone AcetyltransferasesHistone Deacetylase 1Histone DeacetylasesMyoD ProteinNuclear Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsTrans-ActivatorsTranscription Factors

Identifiers

PMID11285237
PMCPMC145490
OpenAlexW2052799089

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.