Evidence map›Paper›PMID 17213813›Full record

ArticleOncogene2007

Disparity of histone deacetylase inhibition on repair of radiation-induced DNA damage on euchromatin and constitutive heterochromatin compartments.

T C Karagiannis, K N Harikrishnan, H Kn, A El-Osta

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.4field-weighted citation impact, top 7% 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, 74 citations in OpenAlex.

  1. Article
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  4. Article
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  7. Article
  8. Knockdown of Rad9A enhanced DNA damage induced by trichostatin A in esophageal cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  9. Article
  10. Bleomycin-induced γH2AX foci map preferentially to replicating domains in CHO9 interphase nuclei.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2014
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Enhanced radiosensitivity of EC109 cells by inhibition of HDAC1 expression.Medical oncology (Northwood, London, England) · 2012
    Article
  16. Is DNA damage response ready for action anywhere?International journal of molecular sciences · 2012
    Review
  17. Review
  18. Article
  19. Article
  20. Potential non-oncological applications of histone deacetylase inhibitors.American journal of translational research · 2011
    Article
4 · The record

Corrections and comments

  • Erratum issued
    Kn, H [corrected to Harikrishnan, K N]
5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

T C KaragiannisTrescowthick Research Laboratories, Department of Molecular Radiation Biology, Peter MacCallum Cancer Centre, East Melbourne, Australia.
K N Harikrishnan
H Kn
A El-Osta
Baker Heart and Diabetes Institute · AUThe Alfred Hospital · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic regulation of chromatin structure is central to the process of DNA repair. A well-characterized epigenetic feature is the dynamic phosphorylation of the histone H2AX (gammaH2AX) and mobilization of double strand break (DSB) recognition and repair factors to the site. How chromatin structure is altered in response to DNA damage and how such alterations influence DSB repair mechanisms are currently relevant issues. Despite the clear link between histone deacetylases (HDACs) and radiosensitivity, how histone hyperacetylation influence DSB repair remains poorly understood. We have determined the structure of chromatin is a major factor determining radiosensitivity and repair in human cells. Trichostatin A (TSA) enhances radiosensitivity with dose modification factors of 1.2 and 1.9 at 0.2 and 1 microM, respectively. Cells treated with TSA causing hyperacetylation and remodelling on euchromatic alleles coexist with gammaH2AX accumulation in radiosensitized cells. Formation of gammaH2AX on heterochromatin was significantly reduced even when cells were treated with TSA, suggesting that chromatin structure and histone hyperacetylation are pronounced features of radiation sensitivity and repair in euchromatic regions.

Indexed as

DNA DamageHistone Deacetylase InhibitorsAcetylationBlotting, WesternCaspasesCell CycleCell SurvivalChromatin ImmunoprecipitationDNA Breaks, Double-StrandedDNA, NeoplasmDNA RepairDose-Response Relationship, DrugEnzyme InhibitorsEuchromatinHeterochromatinHistone DeacetylasesCaspasesDNA, NeoplasmEnzyme InhibitorsEuchromatinHeterochromatinHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic Acidstrichostatin A

Identifiers

PMID17213813
OpenAlexW1988284872

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.