Evidence map›Paper›PMID 26625199›Full record

ArticleOncotarget2016

Human T-cell leukemia virus type-1-encoded protein HBZ represses p53 function by inhibiting the acetyltransferase activity of p300/CBP and HBO1.

Diana G Wright, Claire Marchal, Kimson Hoang, John A Ankney, Stephanie T Nguyen, Amanda W Rushing, Nicholas Polakowski, Benoit Miotto, Isabelle Lemasson

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.International journal of molecular sciences · 2021
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  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

9 authors at 3 institutions in 2 countries.

Diana G WrightBrody School of Medicine, Department of Microbiology and Immunology, East Carolina University, Greenville, NC, USA.
Claire MarchalUniversité Paris Diderot, Sorbonne Paris Cité, Epigenetics and Cell Fate, UMR 7216, CNRS, Paris, France.
Kimson HoangBrody School of Medicine, Department of Microbiology and Immunology, East Carolina University, Greenville, NC, USA.
John A AnkneyBrody School of Medicine, Department of Microbiology and Immunology, East Carolina University, Greenville, NC, USA.
Stephanie T NguyenBrody School of Medicine, Department of Microbiology and Immunology, East Carolina University, Greenville, NC, USA.
Amanda W RushingBrody School of Medicine, Department of Microbiology and Immunology, East Carolina University, Greenville, NC, USA.
Nicholas PolakowskiBrody School of Medicine, Department of Microbiology and Immunology, East Carolina University, Greenville, NC, USA.
Benoit MiottoUniversité Paris Diderot, Sorbonne Paris Cité, Epigenetics and Cell Fate, UMR 7216, CNRS, Paris, France.
Isabelle LemassonBrody School of Medicine, Department of Microbiology and Immunology, East Carolina University, Greenville, NC, USA.
East Carolina University · USCentre National de la Recherche Scientifique · FRInserm · FR

Funding

Regulation of HTLV-1 and cellular gene transcription by the viral protein HBZR01CA128800 · NCI · EAST CAROLINA UNIVERSITY · PI LEMASSON, ISABELLE MICHELE · 2010 to 2014
$1.3M
NCI NIH HHS CA128800NCI NIH HHS R01 CA128800
6 · The paper itself

Abstract

Adult T-cell leukemia (ATL) is an often fatal malignancy caused by infection with the complex retrovirus, human T-cell Leukemia Virus, type 1 (HTLV-1). In ATL patient samples, the tumor suppressor, p53, is infrequently mutated; however, it has been shown to be inactivated by the viral protein, Tax. Here, we show that another HTLV-1 protein, HBZ, represses p53 activity. In HCT116 p53+/+ cells treated with the DNA-damaging agent, etoposide, HBZ reduced p53-mediated activation of p21/CDKN1A and GADD45A expression, which was associated with a delay in G2 phase-arrest. These effects were attributed to direct inhibition of the histone acetyltransferase (HAT) activity of p300/CBP by HBZ, causing a reduction in p53 acetylation, which has be linked to decreased p53 activity. In addition, HBZ bound to, and inhibited the HAT activity of HBO1. Although HBO1 did not acetylate p53, it acted as a coactivator for p53 at the p21/CDKN1A promoter. Therefore, through interactions with two separate HAT proteins, HBZ impairs the ability of p53 to activate transcription. This mechanism may explain how p53 activity is restricted in ATL cells that do not express Tax due to modifications of the HTLV-1 provirus, which accounts for a majority of patient samples.

Indexed as

AcetylationAnimalsBasic-Leucine Zipper Transcription FactorsBlotting, WesternCell Cycle ProteinsCell Line, TumorCyclin-Dependent Kinase Inhibitor p21EtoposideG2 Phase Cell Cycle CheckpointsGADD45 ProteinsGene Expression Regulation, NeoplasticHCT116 CellsHEK293 CellsHeLa CellsHistone AcetyltransferasesHumansBasic-Leucine Zipper Transcription FactorsCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21EtoposideGADD45A protein, humanGADD45 ProteinsHBZ protein, human T-cell leukemia virus type IHistone AcetyltransferasesKAT7 protein, humanNuclear Proteinsp300-CBP Transcription FactorsRetroviridae ProteinsTumor Suppressor Protein p53adult T-cell leukemiaHBZhistone acetyl transferase activityhuman T-cell leukemia virus type-1p53

Identifiers

PMID26625199
PMCPMC4811490
OpenAlexW2308349995

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.