Evidence map›Paper›PMID 15169878›Full record

ArticleMolecular and cellular biology2004

Activation of the growth-differentiation factor 11 gene by the histone deacetylase (HDAC) inhibitor trichostatin A and repression by HDAC3.

Xiaohong Zhang, Walker Wharton, Zhigang Yuan, Shih-Chang Tsai, Nancy Olashaw, Edward Seto

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 93 citations in OpenAlex.

  1. Trial
  2. GDF11: A promising new drug target for pulmonary fibrosis?Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  3. Article
  4. GDF11: An emerging therapeutic target for liver diseases and fibrosis.Journal of cellular and molecular medicine · 2024
    Review
  5. Article
  6. HDAC3 Knockdown Dysregulates Juvenile Hormone and Apoptosis-Related Genes inInternational journal of molecular sciences · 2022
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Anti-Aging Effects of GDF11 on Skin.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. The versatility and paradox of GDF 11.Pharmacology & therapeutics · 2017
    Review
  19. Article
  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

6 authors at 1 institution in 1 country.

Xiaohong ZhangH. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Walker Wharton
Zhigang Yuan
Shih-Chang Tsai
Nancy Olashaw
Edward Seto
Moffitt Cancer Center · US

Funding

FUNCTIONAL ANALYSIS OF MAMMALIAN HISTONE DEACETYLASESR01GM058486 · NIGMS · UNIVERSITY OF SOUTH FLORIDA · PI SETO, EDWARD · 1999 to 2006
$2.3M
Mechanisms of Transcription Factor Yin Yang 1R01GM064850 · NIGMS · UNIVERSITY OF SOUTH FLORIDA · PI SETO, EDWARD · 2002 to 2005
$1.0M
NIGMS NIH HHS GM58486NIGMS NIH HHS GM64850NIGMS NIH HHS R01 GM058486NIGMS NIH HHS R01 GM064850
6 · The paper itself

Abstract

Histone deacetylase (HDAC) inhibitors inhibit the proliferation of transformed cells in vitro, restrain tumor growth in animals, and are currently being actively exploited as potential anticancer agents. To identify gene targets of the HDAC inhibitor trichostatin A (TSA), we compared the gene expression profiles of BALB/c-3T3 cells treated with or without TSA. Our results show that TSA up-regulates the expression of the gene encoding growth-differentiation factor 11 (Gdf11), a transforming growth factor beta family member that inhibits cell proliferation. Detailed analyses indicated that TSA activates the gdf11 promoter through a conserved CCAAT box element. A comprehensive survey of human HDACs revealed that HDAC3 is necessary and sufficient for the repression of gdf11 promoter activity. Chromatin immunoprecipitation assays showed that treatment of cells with TSA or silencing of HDAC3 expression by small interfering RNA causes the hyperacetylation of Lys-9 in histone H3 on the gdf11 promoter. Together, our results provide a new model in which HDAC inhibitors reverse abnormal cell growth by inactivation of HDAC3, which in turn leads to the derepression of gdf11 expression.

Indexed as

Histone Deacetylase InhibitorsAcetylationAnimalsBALB 3T3 CellsBase SequenceBone Morphogenetic ProteinsCell LineDNA, ComplementaryEnzyme InhibitorsGene Expression RegulationGene SilencingGrowth Differentiation FactorsHeLa CellsHistone Deacetylase 3Histone DeacetylasesHistonesBone Morphogenetic ProteinsDNA, ComplementaryEnzyme InhibitorsGDF11 protein, humanGdf11 protein, mouseGrowth Differentiation FactorsHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHistonesHydroxamic AcidsLysineRNA, MessengerRNA, Small Interferingtrichostatin A

Identifiers

PMID15169878
PMCPMC419886
OpenAlexW2137214629

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.