Evidence map›Paper›PMID 10567539›Full record

ArticleMolecular and cellular biology1999

PCAF interacts with tax and stimulates tax transactivation in a histone acetyltransferase-independent manner.

H Jiang, H Lu, R L Schiltz, C A Pise-Masison, V V Ogryzko, Y Nakatani, J N Brady

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

81 citing papers in PubMed, 134 citations in OpenAlex.

  1. Review
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  3. Review
  4. Article
  5. Yin Yang 1 is a potent activator of human T lymphotropic virus type 1 LTR-driven gene expression via RNA binding.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  6. Review
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  8. Article
  9. Review
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  13. Oncogenes and RNA splicing of human tumor viruses.Emerging microbes & infections · 2014
    Review
  14. Epigenetics, drugs of abuse, and the retroviral promoter.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

21 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

H JiangVirus Tumor Biology Section, Laboratory of Receptor Biology and Gene Expression, Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
H Lu
R L Schiltz
C A Pise-Masison
V V Ogryzko
Y Nakatani
J N Brady
National Institutes of Health · USEunice Kennedy Shriver National Institute of Child Health and Human Development · USGeorge Washington University · US

Funding

INTERACTION OF HTLV-I TAX WITH CELLULAR REGULATORY PROTEINSZ01BC005691 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 1996 to 2008
$2.3M
Inhibition of p53 Tumor Suppressor Function by HTLV-IZIABC005691 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 2009 to 2009
$709k
6 · The paper itself

Abstract

Recent studies have shown that the p300/CREB binding protein (CBP)-associated factor (PCAF) is involved in transcriptional activation. PCAF activity has been shown strongly associated with histone acetyltransferase (HAT) activity. In this report, we present evidence for a HAT-independent transcription function that is activated in the presence of the human T-cell leukemia virus type 1 (HTLV-1) Tax protein. In vitro and in vivo GST-Tax pull-down and coimmunoprecipitation experiments demonstrate that there is a direct interaction between Tax and PCAF, independent of p300/CBP. PCAF can be recruited to the HTLV-1 Tax responsive element in the presence of Tax, and PCAF cooperates with Tax in vivo to activate transcription from the HTLV-1 LTR over 10-fold. Point mutations at Tax amino acid 318 (TaxS318A) or 319 to 320 (Tax M47), which have decreased or no activity on the HTLV-1 promoter, are defective for PCAF binding. Strikingly, the ability of PCAF to stimulate Tax transactivation is not solely dependent on the PCAF HAT domain. Two independent PCAF HAT mutants, which knock out acetyltransferase enzyme activity, activate Tax transactivation to approximately the same level as wild-type PCAF. In contrast, p300 stimulation of Tax transactivation is HAT dependent. These studies provide experimental evidence that PCAF contains a coactivator transcription function independent of the HAT activity on the viral long terminal repeat.

Indexed as

Gene Expression Regulation, ViralSaccharomyces cerevisiae ProteinsTranscriptional ActivationAcetyltransferasesBinding SitesCell Cycle ProteinsCREB-Binding ProteinDNA, ViralGene Products, taxHistone AcetyltransferasesHumansHuman T-lymphotropic virus 1Nuclear Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsRecombinant Fusion ProteinsAcetyltransferasesCell Cycle ProteinsCREB-Binding ProteinCREBBP protein, humanDNA, ViralGene Products, taxHistone AcetyltransferasesNuclear Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsRecombinant Fusion ProteinsSaccharomyces cerevisiae ProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID10567539
PMCPMC84898
OpenAlexW2124135408

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.