Evidence map›Paper›PMID 10611310›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

DNA double-strand break repair proteins are required to cap the ends of mammalian chromosomes.

S M Bailey, J Meyne, D J Chen, A Kurimasa, G C Li, B E Lehnert, E H Goodwin

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed
14.6field-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

144 citing papers in PubMed, 396 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Telomere Aberration Detection by PNA FISH Probe.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  6. Article
  7. Article
  8. Poly(ADP-ribose) polymerase enzymes and the maintenance of genome integrity.Cellular and molecular life sciences : CMLS · 2020
    Review
  9. Review
  10. Review
  11. Review
  12. Telomere length as a potential biomarker of coronary artery disease.The Indian journal of medical research · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

84 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

7 authors at 3 institutions in 1 country.

S M BaileyLife Sciences Division, Los Alamos National Laboratory, MS M888, Los Alamos, NM 87545, USA.
J Meyne
D J Chen
A Kurimasa
G C Li
B E Lehnert
E H Goodwin
Lawrence Berkeley National Laboratory · USLos Alamos National Laboratory · USMemorial Sloan Kettering Cancer Center · US

Funding

Roles of DNA PK in DNA Double Strand Break RepairR37CA050519 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI CHEN, DAVID J · 2003 to 2011
$3.5M
HYPERTHERMIA AND THE FUNCTIONS OF HSP70R01CA056909 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI LI, GLORIA C · 1991 to 2007
$2.0M
ROLES OF DNA PK IN DNA DOUBLE STRAND BREAK REPAIRR01CA050519 · NCI · UNIVERSITY OF CALIF-LOS ALAMOS NAT LAB · PI CHEN, DAVID J · 1989 to 2001
$946k
DNA PK IN RADIATION DAMAGE REPAIR AND LYMPHOMAGENESISR01CA078497 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI LI, GLORIA C · 1998 to 2002
$793k
NCI NIH HHS CA50519NCI NIH HHS CA56909NCI NIH HHS CA78497NCI NIH HHS R01 CA050519NCI NIH HHS R01 CA056909NCI NIH HHS R37 CA050519
6 · The paper itself

Abstract

Recent findings intriguingly place DNA double-strand break repair proteins at chromosome ends in yeast, where they help maintain normal telomere length and structure. In the present study, an essential telomere function, the ability to cap and thereby protect chromosomes from end-to-end fusions, was assessed in repair-deficient mouse cell lines. By using fluorescence in situ hybridization with a probe to telomeric DNA, spontaneously occurring chromosome aberrations were examined for telomere signal at the points of fusion, a clear indication of impaired end-capping. Telomeric fusions were not observed in any of the repair-proficient controls and occurred only rarely in a p53 null mutant. In striking contrast, chromosomal end fusions that retained telomeric sequence were observed in nontransformed DNA-PK(cs)-deficient cells, where they were a major source of chromosomal instability. Metacentric chromosomes created by telomeric fusion became even more abundant in these cells after spontaneous immortalization. Restoration of repair proficiency through transfection with a functional cDNA copy of the human DNA-PK(cs) gene reduced the number of fusions compared with a negative transfection control. Virally transformed cells derived from Ku70 and Ku80 knockout mice also displayed end-to-end fusions. These studies demonstrate that DNA double-strand break repair genes play a dual role in maintaining chromosomal stability in mammalian cells, the known role in repairing incidental DNA damage, as well as a new protective role in telomeric end-capping.

Indexed as

Antigens, NuclearChromosome AberrationsDNA HelicasesDNA RepairSaccharomyces cerevisiae ProteinsAnimalsCell Transformation, ViralDNA-Binding ProteinsIn Situ Hybridization, FluorescenceKu AutoantigenMaleMiceMice, Inbred StrainsMice, KnockoutNuclear ProteinsTelomereAntigens, NuclearDNA-Binding ProteinsDNA Helicaseshigh affinity DNA-binding factor, S cerevisiaeKu AutoantigenNuclear ProteinsSaccharomyces cerevisiae ProteinsTelomeric Repeat Binding Protein 2XRCC5 protein, humanXrcc6 protein, humanXrcc6 protein, mouse

Identifiers

PMID10611310
PMCPMC24745
OpenAlexW2158820560

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.