Evidence map›Paper›PMID 14968110›Full record

ArticleOncogene2004

Deacetylase recruitment by the C/H3 domain of the acetyltransferase p300.

Cristiano Simone, Peter Stiegler, Sonia-Vanina Forcales, Luigi Bagella, Antonio De Luca, Vittorio Sartorelli, Antonio Giordano, Pier Lorenzo Puri

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Epigenetic mechanisms in learned fear: implications for PTSD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013
    Review
  9. Article
  10. Review
  11. Review
  12. Role of HDAC1 in senescence, aging, and cancer.Experimental gerontology · 2010
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Effects of histone deacetylase inhibitors on HIF-1.Cell cycle (Georgetown, Tex.) · 2006
    Review
  19. Review
  20. 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

8 authors at 5 institutions in 2 countries.

Cristiano SimoneLaboratory of Gene Expression, Dulbecco Telethon Institute (DTI) at Fondazione A Cesalpino, University of Roma La Sapienza, Italy.
Peter Stiegler
Sonia-Vanina Forcales
Luigi Bagella
Antonio De Luca
Vittorio Sartorelli
Antonio Giordano
Pier Lorenzo Puri
Temple University · USDulbecco Telethon Institute · ITIstituto Neurologico Mediterraneo · ITNational Institutes of Health · USSalk Institute for Biological Studies · US

Funding

Isolation And Characterization Of MyoD-Associated Factors (MAFs)Z01AR041125 · NIAMS · ARTHRITIS, MUSCULOSKELETAL, SKIN DIS · PI SARTORELLI, VITTORIO · 2000 to 2007
$1.4M
Telethon GFP01009
6 · The paper itself

Abstract

The balance between acetylation and deacetylation of histone and nonhistone proteins controls gene expression in a variety of cellular processes, with transcription being activated by acetyltransferases and silenced by deacetylases. We report here the formation and enzymatic characterization of a complex between the acetyltransferase p300 and histone deacetylases. The C/H3 region of p300 was found to co-purify deacetylase activity from nuclear cell extracts. A prototype of class I histone deacetylases, HDAC1, interacts with p300 C/H3 domain in vitro and in vivo. The p300-binding protein E1A competes with HDAC1 for C/H3 binding; and, like E1A, HDAC1 overexpression interferes with either activation of Gal4p300 fusion protein or p300-dependent co-activation of two C/H3-binding proteins, MyoD and p53. The exposure to deacetylase inhibitors could reverse the dominant-negative effect of a C/H3 fragment insulated from the rest of the molecule, on MyoD- and p53-dependent transcription, whereas inhibition by E1A was resistant to trichostatin A. These data support the hypothesis that association between acetyltransferases and deacetylases can control the expression of genes implicated in cellular growth and differentiation, and suggest that the dominant-negative effect of the p300 C/H3 fragment relies on deacetylase recruitment.

Indexed as

AcetyltransferasesAdenovirus E1A ProteinsAnimalsCell LineChlorocebus aethiopsCOS CellsGene Expression RegulationGene Expression Regulation, NeoplasticHeLa CellsHistone Deacetylase 1Histone DeacetylasesHumansMiceMyoD ProteinNIH 3T3 CellsProteinsAcetyltransferasesAdenovirus E1A ProteinsHDAC1 protein, humanHdac1 protein, mouseHistone Deacetylase 1Histone DeacetylasesMyoD ProteinProteinsTumor Suppressor Protein p53

Identifiers

PMID14968110
OpenAlexW2031060077

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.