Evidence map›Paper›PMID 23346550›Full record

ArticleFrontiers in oncology2012

Chromatin modifications and the DNA damage response to ionizing radiation.

Rakesh Kumar, Nobuo Horikoshi, Mayank Singh, Arun Gupta, Hari S Misra, Kevin Albuquerque, Clayton R Hunt, Tej K Pandita

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.7field-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

42 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Mechanisms of DNA Damage Response in Mammalian Oocytes.Advances in anatomy, embryology, and cell biology · 2024
    Review
  6. Article
  7. Review
  8. Preleukemic Fusion Genes Induced via Ionizing Radiation.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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 4 institutions in 2 countries.

Rakesh KumarDepartment of Radiation Oncology, University of Texas Southwestern Medical Center Dallas, TX, USA.
Nobuo Horikoshi
Mayank Singh
Arun Gupta
Hari S Misra
Kevin Albuquerque
Clayton R Hunt
Tej K Pandita
The University of Texas Southwestern Medical Center · USSouthwestern Medical CenterRadiation Oncology Associates · USSouthwestern Medical Center · US

Funding

CHROMATIN MODIFYING FACTORS CONTROL RADIATION RESPONSE AND GENOMIC STABILITYR01CA129537 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2008 to 2018
$3.3M
Tumor-cell-specific targets for combined hyperthermia and radiation effectsR01CA154320 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI PANDITA, TEJ K · 2010 to 2014
$1.6M
Functional Characterization of the Mammalian MOF Gene ProductR01CA123232 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2007 to 2011
$1.5M
NCI NIH HHS R01 CA123232NCI NIH HHS R01 CA129537NCI NIH HHS R01 CA154320
6 · The paper itself

Abstract

In order to survive, cells have evolved highly effective repair mechanisms to deal with the potentially lethal DNA damage produced by exposure to endogenous as well as exogenous agents. Ionizing radiation exposure induces highly lethal DNA damage, especially DNA double-strand breaks (DSBs), that is sensed by the cellular machinery and then subsequently repaired by either of two different DSB repair mechanisms: (1) non-homologous end joining, which re-ligates the broken ends of the DNA and (2) homologous recombination, that employs an undamaged identical DNA sequence as a template, to maintain the fidelity of DNA repair. Repair of DSBs must occur within the natural context of the cellular DNA which, along with specific proteins, is organized to form chromatin, the overall structure of which can impede DNA damage site access by repair proteins. The chromatin complex is a dynamic structure and is known to change as required for ongoing cellular processes such as gene transcription or DNA replication. Similarly, during the process of DNA damage sensing and repair, chromatin needs to undergo several changes in order to facilitate accessibility of the repair machinery. Cells utilize several factors to modify the chromatin in order to locally open up the structure to reveal the underlying DNA sequence but post-translational modification of the histone components is one of the primary mechanisms. In this review, we will summarize chromatin modifications by the respective chromatin modifying factors that occur during the DNA damage response.

Indexed as

DNA repairhistone modifications

Identifiers

PMID23346550
PMCPMC3551241
OpenAlexW2126898119

What OpenQuestion 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 OpenQuestion graph.