Evidence map›Paper›PMID 10734308›Full record

ArticleOncogene2000

HTLV-1 tax oncoprotein represses the p53-mediated trans-activation function through coactivator CBP sequestration.

Y Ariumi, A Kaida, J Y Lin, M Hirota, O Masui, S Yamaoka, Y Taya, K Shimotohno

Abstract read
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In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

65 citing papers in PubMed, 117 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020
    Review
  7. Review
  8. Review
  9. Article
  10. HIV-1 Vpr and p21 restrict LINE-1 mobility.Nucleic acids research · 2018
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

5 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

8 authors at 2 institutions in 1 country.

Y AriumiInstitute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.
A Kaida
J Y Lin
M Hirota
O Masui
S Yamaoka
Y Taya
K Shimotohno
Kyoto University · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein repressed the transcriptional activity of wild-type p53 through its N-terminal trans-activation domain. Although Tax did not directly bind to p53, this repression required the activation of CREB pathway by Tax. In contrast to a recent report by Pise-Masison et al. (1998a, b) we found that the phosphorylation of p53 on Ser 15 is not a major cause of the Tax-mediated inactivation of p53. However, Tax with a mutation in the coactivator CBP-binding site (K88A), which activates NF-kappaB but not the CREB pathway, could not repress the p53 trans-activation function. Moreover, Tax inhibited p53 binding to CBP in vitro and inhibited synergistic activation of transcription by CBP and p53. Thus, Tax is likely to compete with p53 in binding with CBP, thereby repressing its trans-activation function.

Indexed as

Binding, CompetitiveCell LineCREB-Binding ProteinCyclic AMP Response Element-Binding ProteinGene Products, taxGene SilencingHumansNF-kappa BNuclear ProteinsPhosphorylationTrans-ActivatorsTranscription, GeneticTumor Suppressor Protein p53CREB-Binding ProteinCREBBP protein, humanCyclic AMP Response Element-Binding ProteinGene Products, taxNF-kappa BNuclear ProteinsTrans-ActivatorsTumor Suppressor Protein p53

Identifiers

PMID10734308
OpenAlexW2043331982

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.