Evidence map›Paper›PMID 15870300›Full record

ArticleMolecular and cellular biology2005

TAF1 histone acetyltransferase activity in Sp1 activation of the cyclin D1 promoter.

Traci L Hilton, Yun Li, Elizabeth L Dunphy, Edith H Wang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Harnessing the TAF1 Acetyltransferase for Targeted Acetylation of the Tumor Suppressor p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  6. Review
  7. Article
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  9. Article
  10. A novel variant inNeuronal signaling · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Landscape of somatic single-nucleotide and copy-number mutations in uterine serous carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  18. Article
  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

4 authors at 1 institution in 1 country.

Traci L HiltonUniversity of Washington, School of Medicine, Department of Pharmacology, 1959 NE Pacific Street, Health Sciences Center, Box 357280, Seattle, WA 98195-7280, USA.
Yun Li
Elizabeth L Dunphy
Edith H Wang
University of Washington · US

Funding

TRAINING IN MOLECULAR AND CELLULAR BIOLOGYT32GM007270 · NIGMS · UNIVERSITY OF WASHINGTON · PI RAIBLE, DAVID W · 1985 to 2020
$21.0M
Pharmacological Sciences SupplementT32GM007750 · NIGMS · UNIVERSITY OF WASHINGTON · PI ATKINS, WILLIAM M · 1985 to 2023
$12.6M
NIGMS NIH HHS GM7750NIGMS NIH HHS T32 GM007270NIGMS NIH HHS T32 GM007750NIGMS NIH HHS T32 GM07270
6 · The paper itself

Abstract

A missense mutation within the histone acetyltransferase (HAT) domain of the TATA binding protein-associated factor TAF1 induces ts13 cells to undergo a late G(1) arrest and decreases cyclin D1 transcription. We have found that TAF1 mutants (Delta844-850 and Delta848-850, from which amino acids 844 through 850 and 848 through 850 have been deleted, respectively) deficient in HAT activity are unable to complement the ts13 defect in cell proliferation and cyclin D1 transcription. Chromatin immunoprecipitation assays revealed that histone H3 acetylation was reduced at the cyclin D1 promoter but not the c-fos promoter upon inactivation of TAF1 in ts13 cells. The hypoacetylation of H3 at the cyclin D1 promoter was reversed by treatment with trichostatin A (TSA), a histone deacetylase inhibitor, or by expression of TAF1 proteins that retain HAT activity. Transcription of a chimeric promoter containing the Sp1 sites of cyclin D1 and c-fos core remained TAF1 dependent in ts13 cells. Treatment with TSA restored full activity to the cyclin D1-c-fos chimera at 39.5 degrees C. In vivo genomic footprinting experiments indicate that protein-DNA interactions at the Sp1 sites of the cyclin D1 promoter were compromised at 39.5 degrees C in ts13 cells. These data have led us to hypothesize that TAF1-dependent histone acetylation facilitates transcription factor binding to the Sp1 sites, thereby activating cyclin D1 transcription and ultimately G(1)-to-S-phase progression.

Indexed as

AcetylationAcetyltransferasesAmino Acid SequenceBase SequenceCell LineCyclin D1Genetic Complementation TestHistone AcetyltransferasesHistonesHumansMolecular Sequence DataMutationPhenotypePromoter Regions, GeneticProtein Structure, TertiaryResponse ElementsAcetyltransferasesCyclin D1Histone AcetyltransferasesHistonesSp1 Transcription FactorTATA-binding protein associated factor 250 kDaTATA-Binding Protein Associated FactorsTranscription Factor TFIID

Identifiers

PMID15870300
PMCPMC1087727
OpenAlexW2119793417

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.