Evidence map›Paper›PMID 9620779›Full record

ArticleNature genetics1998

Methylated DNA and MeCP2 recruit histone deacetylase to repress transcription.

P L Jones, G J Veenstra, P A Wade, D Vermaak, S U Kass, N Landsberger, J Strouboulis, A P Wolffe

Abstract read
PubMed Publisher
In one paragraph

Article in Nature genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 960 papers.

0numbers the graph read from it
0cells of the map it votes in
960citing papers in PubMed
52.8field-weighted citation impact, top 1% 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

960 citing papers in PubMed, 2,718 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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  19. All-in-one vectors for epigenetic CRISPR inhibition ofMolecular therapy. Methods & clinical development · 2025
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  20. Article

900 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

8 authors at 3 institutions in 2 countries.

P L JonesLaboratory of Molecular Embryology, National Institute of Child Health and Human Development, National Institute of Health, Bethesda, Maryland 20892-5431, USA.
G J Veenstra
P A Wade
D Vermaak
S U Kass
N Landsberger
J Strouboulis
A P Wolffe
National Institutes of Health · USEunice Kennedy Shriver National Institute of Child Health and Human Development · USJanssen (Belgium) · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CpG methylation in vertebrates correlates with alterations in chromatin structure and gene silencing. Differences in DNA-methylation status are associated with imprinting phenomena and carcinogenesis. In Xenopus laevis oocytes, DNA methylation dominantly silences transcription through the assembly of a repressive nucleosomal array. Methylated DNA assembled into chromatin binds the transcriptional repressor MeCP2 which cofractionates with Sin3 and histone deacetylase. Silencing conferred by MeCP2 and methylated DNA can be relieved by inhibition of histone deacetylase, facilitating the remodelling of chromatin and transcriptional activation. These results establish a direct causal relationship between DNA methylation-dependent transcriptional silencing and the modification of chromatin.

Indexed as

Chromosomal Proteins, Non-HistoneDNA MethylationSaccharomyces cerevisiae ProteinsTranscription, GeneticAmino Acid SequenceAnimalsBinding SitesDNA-Binding ProteinsHistone DeacetylasesMethyl-CpG-Binding Protein 2Molecular Sequence DataRepressor ProteinsTranscription FactorsXenopus laevisXenopus ProteinsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsHistone DeacetylasesMECP2 protein, XenopusMethyl-CpG-Binding Protein 2Repressor ProteinsSaccharomyces cerevisiae ProteinsSIN3 protein, S cerevisiaeTranscription FactorsXenopus Proteins

Identifiers

PMID9620779
OpenAlexW1486257535

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.