Evidence map›Paper›PMID 23589625›Full record

ArticleNucleic acids research2013

HP1 promotes tumor suppressor BRCA1 functions during the DNA damage response.

Young-Ho Lee, Ching-Ying Kuo, Jeremy M Stark, Hsiu-Ming Shih, David K Ann

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

7 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

5 authors at 3 institutions in 1 country.

Young-Ho LeeDepartment of Molecular Pharmacology, Beckman Research Institute, City of Hope, Duarte, CA 91010, USA.
Ching-Ying Kuo
Jeremy M Stark
Hsiu-Ming Shih
David K Ann
City of Hope · USCity Of Hope National Medical Center · USBeckman Research Institute

Funding

MOLECULAR PROGRAMMING OF SALIVARY GLAND GENE EXPRESSIONR01DE010742 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANN, DAVID K. · 1993 to 2013
$5.1M
Molecular Hierarchies in Salivary Adaptive ResponsesR01DE014183 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANN, DAVID K. · 2001 to 2011
$3.3M
Mechanistic steps of homologous repair in mammalian cellsR01CA120954 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI STARK, JEREMY MICHAEL · 2006 to 2016
$2.2M
NCI NIH HHS R01 CA120954NCI NIH HHS R01CA120954NIDCR NIH HHS R01 DE010742NIDCR NIH HHS R01DE10742NIDCR NIH HHS R01DE14183
6 · The paper itself

Abstract

The DNA damage response (DDR) involves both the control of DNA damage repair and signaling to cell cycle checkpoints. Therefore, unraveling the underlying mechanisms of the DDR is important for understanding tumor suppression and cellular resistance to clastogenic cancer therapeutics. Because the DDR is likely to be influenced by chromatin regulation at the sites of DNA damage, we investigated the role of heterochromatin protein 1 (HP1) during the DDR process. We monitored double-strand breaks (DSBs) using the γH2AX foci marker and found that depleting cells of HP1 caused genotoxic stress, a delay in the repair of DSBs and elevated levels of apoptosis after irradiation. Furthermore, we found that these defects in repair were associated with impaired BRCA1 function. Depleting HP1 reduced recruitment of BRCA1 to DSBs and caused defects in two BRCA1-mediated DDR events: (i) the homologous recombination repair pathway and (ii) the arrest of cell cycle at the G2/M checkpoint. In contrast, depleting HP1 from cells did not affect the non-homologous end-joining (NHEJ) pathway: instead it elevated the recruitment of the 53BP1 NHEJ factor to DSBs. Notably, all three subtypes of HP1 seemed to be almost equally important for these DDR functions. We suggest that the dynamic interaction of HP1 with chromatin and other DDR factors could determine DNA repair choice and cell fate after DNA damage. We also suggest that compromising HP1 expression could promote tumorigenesis by impairing the function of the BRCA1 tumor suppressor.

Indexed as

Recombinational DNA RepairApoptosisBRCA1 ProteinCell Cycle CheckpointsCell LineCell ProliferationChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNA DamageDNA End-Joining RepairHumansIntracellular Signaling Peptides and ProteinsMCF-7 CellsRadiation, IonizingTumor Suppressor p53-Binding Protein 1BRCA1 ProteinChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneIntracellular Signaling Peptides and ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1

Identifiers

PMID23589625
PMCPMC3675466
OpenAlexW1990672687

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.