Evidence map›Paper›PMID 23916969›Full record

ReviewMutation research2013

Double strand break repair functions of histone H2AX.

Ralph Scully, Anyong Xie

Open access · greenAbstract readReview
In one paragraph

Review in Mutation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 247 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Cancer nanotechnology · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Potential Noninvasive Biomarkers to Assess the Aging Process.Expert reviews in molecular medicine · 2025
    Review
  15. Cholangiocytes' primary cilia regulate DNA damage response and repair.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Article
  16. Article
  17. Wogonin inhibits radiation-induced DNA damage repair in hepatocellular carcinoma cells by upregulating p21.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  18. Article
  19. Article
  20. Article

65 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

2 authors at 1 institution in 1 country.

Ralph ScullyDepartment of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, United States. Electronic address: rscully@bidmc.harvard.edu.
Anyong Xie
Beth Israel Deaconess Medical Center · US

Funding

ANALYSIS OF BRCA1 RECOMBINATION FUNCTIONSR01CA095175 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SCULLY, RALPH · 2002 to 2021
$4.9M
The chromatin response in mammalian double strand break repairR01GM073894 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SCULLY, RALPH · 2005 to 2014
$2.5M
Targeting non-homologous end joining in cancer therapyRC1CA145867 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SCULLY, RALPH · 2009 to 2010
$1.0M
NCI NIH HHS CA095175NCI NIH HHS R01 CA095175NCI NIH HHS RC1 CA145867NIGMS NIH HHS GM073894NIGMS NIH HHS R01 GM073894
6 · The paper itself

Abstract

Chromosomal double strand breaks provoke an extensive reaction in neighboring chromatin, characterized by phosphorylation of histone H2AX on serine 139 of its C-terminal tail (to form "γH2AX"). The γH2AX response contributes to the repair of double strand breaks encountered in a variety of different contexts, including those induced by ionizing radiation, physiologically programmed breaks that characterize normal immune cell development and the pathological exposure of DNA ends triggered by telomere dysfunction. γH2AX also participates in the evolutionarily conserved process of sister chromatid recombination, a homologous recombination pathway involved in the suppression of genomic instability during DNA replication and directly implicated in tumor suppression. At a biochemical level, the γH2AX response provides a compelling example of how the "histone code" is adapted to the regulation of double strand break repair. Here, we review progress in research aimed at understanding how γH2AX contributes to double strand break repair in mammalian cells.

Indexed as

DNA Breaks, Double-StrandedAnimalsBinding SitesChromatinDNA RepairHistonesHumansIntracellular Signaling Peptides and ProteinsModels, GeneticTumor Suppressor p53-Binding Protein 1ChromatinH2AX protein, humanHistonesIntracellular Signaling Peptides and ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 153BP1BRCA1H2AXHistone codeHomologous recombinationMammalian DSB repairMDC1Mre11/Rad50/Nbs1Non-homologous end joiningSingle strand annealing

Identifiers

PMID23916969
PMCPMC3818383
OpenAlexW1968073368

What OpenQuestion holds

Textmetadata
LicenceTDM
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.