Evidence map›Paper›PMID 12032080›Full record

ArticleThe EMBO journal2002

Essential function of histone deacetylase 1 in proliferation control and CDK inhibitor repression.

Gerda Lagger, Dónal O'Carroll, Martina Rembold, Harald Khier, Julia Tischler, Georg Weitzer, Bernd Schuettengruber, Christoph Hauser, Reinhard Brunmeir, Thomas Jenuwein and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 378 papers.

0numbers the graph read from it
0cells of the map it votes in
378citing papers in PubMed
9.2field-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

378 citing papers in PubMed, 756 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  9. Article
  10. Article
  11. Feto-placental blood vessel development.Development (Cambridge, England) · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Critical Windows: Exploring the Association Between Perinatal Trauma, Epigenetics, and Chronic Pain.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  18. Article
  19. Review
  20. Article

318 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

11 authors at 1 institution in 1 country.

Gerda LaggerInstitute of Medical Biochemistry, Division of Molecular Biology, University of Vienna, Vienna Biocenter, Dr Bohr-Gasse 9/2, A-1030 Vienna, Austria.
Dónal O'Carroll
Martina Rembold
Harald Khier
Julia Tischler
Georg Weitzer
Bernd Schuettengruber
Christoph Hauser
Reinhard Brunmeir
Thomas Jenuwein
Christian Seiser
Research Institute of Molecular Pathology · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylases (HDACs) modulate chromatin structure and transcription, but little is known about their function in mammalian development. HDAC1 was implicated previously in the repression of genes required for cell proliferation and differentiation. Here we show that targeted disruption of both HDAC1 alleles results in embryonic lethality before E10.5 due to severe proliferation defects and retardation in development. HDAC1-deficient embryonic stem cells show reduced proliferation rates, which correlate with decreased cyclin-associated kinase activities and elevated levels of the cyclin-dependent kinase inhibitors p21(WAF1/CIP1) and p27(KIP1). Similarly, expression of p21 and p27 is up-regulated in HDAC1-null embryos. In addition, loss of HDAC1 leads to significantly reduced overall deacetylase activity, hyperacetylation of a subset of histones H3 and H4 and concomitant changes in other histone modifications. The expression of HDAC2 and HDAC3 is induced in HDAC1-deficient cells, but cannot compensate for loss of the enzyme, suggesting a unique function for HDAC1. Our study provides the first evidence that a histone deacetylase is essential for unrestricted cell proliferation by repressing the expression of selective cell cycle inhibitors.

Indexed as

AllelesAnimalsBlotting, SouthernBlotting, WesternCell Cycle ProteinsCell DivisionCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesCyclinsExonsHistone Deacetylase 1Histone DeacetylasesHistonesIn Situ HybridizationIn Situ Nick-End LabelingCdkn1a protein, mouseCdkn1b protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesCyclinsHDAC1 protein, humanHistone Deacetylase 1Histone DeacetylasesHistonesTumor Suppressor Proteins

Identifiers

PMID12032080
PMCPMC126040
OpenAlexW1910848366

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.