Evidence map›Paper›PMID 20729195›Full record

ArticleThe Journal of biological chemistry2010

The viral oncoprotein tax sequesters DNA damage response factors by tethering MDC1 to chromatin.

S Mehdi Belgnaoui, Kimberly A Fryrear, Julius O Nyalwidhe, Xin Guo, O John Semmes

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Regulation of HTLV-1 transformation.Bioscience reports · 2022
    Review
  4. Review
  5. Review
  6. Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020
    Review
  7. Article
  8. Interplay Between KSHV and the Host DNA Damage Response.Frontiers in cellular and infection microbiology · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. CHK2 kinase in the DNA damage response and beyond.Journal of molecular cell biology · 2014
    Review
  16. Article
  17. Review
  18. Review
  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

5 authors at 1 institution in 1 country.

S Mehdi BelgnaouiFrom the Department of Microbiology and Molecular Cell Biology, Cancer Biology and Infectious Disease Research Center, Eastern Virginia Medical School, Norfolk, Virgina 23508.
Kimberly A FryrearFrom the Department of Microbiology and Molecular Cell Biology, Cancer Biology and Infectious Disease Research Center, Eastern Virginia Medical School, Norfolk, Virgina 23508.
Julius O NyalwidheFrom the Department of Microbiology and Molecular Cell Biology, Cancer Biology and Infectious Disease Research Center, Eastern Virginia Medical School, Norfolk, Virgina 23508.
Xin GuoFrom the Department of Microbiology and Molecular Cell Biology, Cancer Biology and Infectious Disease Research Center, Eastern Virginia Medical School, Norfolk, Virgina 23508.
O John SemmesFrom the Department of Microbiology and Molecular Cell Biology, Cancer Biology and Infectious Disease Research Center, Eastern Virginia Medical School, Norfolk, Virgina 23508. Electronic address: Semmesoj@evms.edu.
Eastern Virginia Medical School · US

Funding

HTLV-I TAX MEDIATED DEREGULATION OF CELL STATER01CA076595 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI SEMMES, OLIVER JOHN · 1999 to 2016
$2.9M
PSYCHOSOCIAL SEQUELAE TO PREDISPOSITION GENETIC TESTINGK07CA076959 · NCI · YALE UNIVERSITY · PI PASACRETA, JEANNIE V · 1997 to 2001
$255k
NCI NIH HHS CA76959NCI NIH HHS R01 CA076595
6 · The paper itself

Abstract

Infection with human T-cell leukemia virus induces cellular genomic instability mediated through the viral oncoprotein Tax. Here we present evidence that Tax undermines the cellular DNA damage response by sequestration of damage response factors. We show by confocal microscopy that Tax forms damage-independent nuclear foci that contain DNA-PK, BRCA1, and MDC1. Tax sequesters MDC1 to chromatin sites distinct from classic ionizing radiation-induced foci. The recruitment of MDC1 is competitive between the two foci. The N-terminal region of Tax is sufficient for foci localization, and the C-terminal half is critical for binding to MDC1 and recruitment of additional response factors. Tax expression and DNA damage response factor recruitment repressed the formation of ionizing radiation-induced Nbs1-containing foci. The Tax-induced "pseudo" DNA damage response results in phosphorylation and monoubiquitylation of H2AX, which is ablated by siRNA suppression of MDC1. These data support a model for virus-induced genomic instability in which viral oncogene-induced damage-independent foci compete with normal cellular DNA damage response.

Indexed as

DNA DamageGenomic InstabilityModels, BiologicalAdaptor Proteins, Signal TransducingBRCA1 ProteinCell Cycle ProteinsCell LineCell NucleusChromatinDNA-Activated Protein KinaseGene Products, taxHumansHuman T-lymphotropic virus 1Nuclear ProteinsPhosphorylationRadiation, IonizingAdaptor Proteins, Signal TransducingBRCA1 ProteinBRCA1 protein, humanCell Cycle ProteinsChromatinDNA-Activated Protein KinaseGene Products, taxMDC1 protein, humanNuclear ProteinsPRKDC protein, humantax protein, Human T-lymphotrophic virus 1Trans-Activators

Identifiers

PMID20729195
PMCPMC2963403
OpenAlexW2077676818

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.