Evidence map›Paper›PMID 19139074›Full record

ReviewNucleic acids research2009

Chromatin remodeling finds its place in the DNA double-strand break response.

Tej K Pandita, Christine Richardson

Open access · goldAbstract readReview
In one paragraph

Review in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

78 citing papers in PubMed, 122 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The Connection Between Cell Fate and Telomere.Advances in experimental medicine and biology · 2021
    Review
  11. Article
  12. Article
  13. Bisphenol B Exposure Disrupts Mouse Oocyte Meiotic MaturationFrontiers in cell and developmental biology · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

18 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 2 institutions in 1 country.

Tej K PanditaDepartment of Radiation Oncology, Washington University School of Medicine, St Louis, MO 63108, USA. pandita@wustl.edu
Christine Richardson
University of North Carolina at Charlotte · USWashington University in St. Louis · US

Funding

CHROMATIN MODIFYING FACTORS CONTROL RADIATION RESPONSE AND GENOMIC STABILITYR01CA129537 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2008 to 2018
$3.3M
Etiology of Translocations in Hematopoietic CellsR01CA100159 · NCI · UNIVERSITY OF NORTH CAROLINA CHARLOTTE · PI RICHARDSON, CHRISTINE A. · 2003 to 2017
$2.4M
Functional Characterization of the Mammalian MOF Gene ProductR01CA123232 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2007 to 2011
$1.5M
Etiology of translocations in hematopoietic cellsR56CA100159 · NCI · UNIVERSITY OF NORTH CAROLINA CHARLOTTE · PI RICHARDSON, CHRISTINE A. · 2008 to 2008
$264k
NCI NIH HHS CA100159NCI NIH HHS CA10445NCI NIH HHS CA123232NCI NIH HHS CA129537
6 · The paper itself

Abstract

The accurate repair of chromosomal double-strand breaks (DSBs) arising from exposure to exogenous agents, such as ionizing radiation (IR) and radiomimetic drugs is crucial in maintaining genomic integrity, cellular viability and the prevention of tumorigenesis. Eukaryotic cells have evolved efficient mechanisms that sense and respond to DSBs. The DNA DSB response is facilitated by hierarchical signaling networks that orchestrate chromatin structural changes, cell-cycle checkpoints and multiple enzymatic activities to repair the broken DNA ends. Sensors and transducers signal to numerous downstream cellular effectors which function primarily by substrate posttranslational modifications including phosphorylation, acetylation, methylation and ubiquitylation. In particular, the past several years have provided important insight into the role of chromatin remodeling and histones-specific modifications to control DNA damage detection, signaling and repair. This review summarizes recently identified factors that influence this complex process and the repair of DNA DSBs in eukaryotic cells.

Indexed as

Chromatin Assembly and DisassemblyDNA Breaks, Double-StrandedDNA RepairAdaptor Proteins, Signal TransducingChromatinGenetic Diseases, InbornHumansMethylationProtein KinasesSignal TransductionUbiquitinationAdaptor Proteins, Signal TransducingChromatinProtein Kinases

Identifiers

PMID19139074
PMCPMC2655678
OpenAlexW2168237762

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.