Evidence map›Paper›PMID 10779327›Full record

ArticleMolecular and cellular biology2000

Inactivation of p53 by human T-cell lymphotropic virus type 1 Tax requires activation of the NF-kappaB pathway and is dependent on p53 phosphorylation.

C A Pise-Masison, R Mahieux, H Jiang, M Ashcroft, M Radonovich, J Duvall, C Guillerm, J N Brady

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
3.8field-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

75 citing papers in PubMed, 138 citations in OpenAlex.

  1. Review
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  14. Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Modulation of p53 during bacterial infections.Nature reviews. Microbiology · 2015
    Review

15 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 3 institutions in 1 country.

C A Pise-MasisonVirus Tumor Biology Section, Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. masionc@dce41.nci.nih.gov
R Mahieux
H Jiang
M Ashcroft
M Radonovich
J Duvall
C Guillerm
J N Brady
National Cancer Institute · USNational Institutes of Health · USFrederick National Laboratory for Cancer Research · 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

p53 plays a key role in guarding cells against DNA damage and transformation. We previously demonstrated that the human T-cell lymphotropic virus type 1 (HTLV-1) Tax can inactivate p53 transactivation function in lymphocytes. The present study demonstrates that in T cells, Tax-induced p53 inactivation is dependent upon NF-kappaB activation. Analysis of Tax mutants demonstrated that Tax inactivation of p53 function correlates with the ability of Tax to induce NF-kappaB but not p300 binding or CREB transactivation. The Tax-induced p53 inactivation can be overcome by overexpression of a dominant IkappaB mutant. Tax-NF-kappaB-induced p53 inactivation is not due to p300 squelching, since overexpression of p300 does not recover p53 activity in the presence of Tax. Further, using wild-type and p65 knockout mouse embryo fibroblasts (MEFs), we demonstrate that the p65 subunit of NF-kappaB is critical for Tax-induced p53 inactivation. While Tax can inactivate endogenous p53 function in wild-type MEFs, it fails to inactivate p53 function in p65 knockout MEFs. Importantly, Tax-induced p53 inactivation can be restored by expression of p65 in the knockout MEFs. Finally, we present evidence that phosphorylation of serines 15 and 392 correlates with inactivation of p53 by Tax in T cells. This study provides evidence that the divergent NF-kappaB proliferative and p53 cell cycle arrest pathways may be cross-regulated at several levels, including posttranslational modification of p53.

Indexed as

AnimalsE1A-Associated p300 ProteinFibroblastsGene Products, taxHumansHuman T-lymphotropic virus 1I-kappa B ProteinsJurkat CellsMiceMice, KnockoutMutationNF-kappa BNuclear ProteinsPhosphorylationT-LymphocytesTrans-ActivatorsE1A-Associated p300 ProteinEp300 protein, mouseGene Products, taxI-kappa B ProteinsNF-kappa BNuclear ProteinsTrans-ActivatorsTranscription Factor RelATumor Suppressor Protein p53

Identifiers

PMID10779327
PMCPMC85630
OpenAlexW2154633327

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.