Evidence map›Paper›PMID 26209132›Full record

ArticleNucleic acids research2015

Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks.

Keiko Muraki, Limei Han, Douglas Miller, John P Murnane

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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

4 authors at 1 institution in 1 country.

Keiko MurakiDepartment of Radiation Oncology, University of California, San Francisco, 2340 Sutter St. San Francisco, CA 94143-1330, USA.
Limei HanDepartment of Radiation Oncology, University of California, San Francisco, 2340 Sutter St. San Francisco, CA 94143-1330, USA.
Douglas MillerDepartment of Radiation Oncology, University of California, San Francisco, 2340 Sutter St. San Francisco, CA 94143-1330, USA.
John P MurnaneDepartment of Radiation Oncology, University of California, San Francisco, 2340 Sutter St. San Francisco, CA 94143-1330, USA JMurnane@radonc.ucsf.edu.
University of California, San Francisco · US

Funding

Chromosome instability resulting from double-strand breaks near telomeresR01CA120205 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MURNANE, JOHN P. · 2006 to 2015
$2.6M
NCI NIH HHS CA120205NCI NIH HHS R01 CA120205
6 · The paper itself

Abstract

The caps on the ends of chromosomes, called telomeres, keep the ends of chromosomes from appearing as DNA double-strand breaks (DSBs) and prevent chromosome fusion. However, subtelomeric regions are sensitive to DSBs, which in normal cells is responsible for ionizing radiation-induced cell senescence and protection against oncogene-induced replication stress, but promotes chromosome instability in cancer cells that lack cell cycle checkpoints. We have previously reported that I-SceI endonuclease-induced DSBs near telomeres in a human cancer cell line are much more likely to generate large deletions and gross chromosome rearrangements (GCRs) than interstitial DSBs, but found no difference in the frequency of I-SceI-induced small deletions at interstitial and subtelomeric DSBs. We now show that inhibition of MRE11 3'-5' exonuclease activity with Mirin reduces the frequency of large deletions and GCRs at both interstitial and subtelomeric DSBs, but has little effect on the frequency of small deletions. We conclude that large deletions and GCRs are due to excessive processing of DSBs, while most small deletions occur during classical nonhomologous end joining (C-NHEJ). The sensitivity of subtelomeric regions to DSBs is therefore because they are prone to undergo excessive processing, and not because of a deficiency in C-NHEJ in subtelomeric regions.

Indexed as

DNA Breaks, Double-StrandedCell Line, TumorChromosome AberrationsDNA-Binding ProteinsDNA End-Joining RepairDNA RepairExodeoxyribonucleasesHumansMRE11 Homologue ProteinMutationPyrimidinonesSequence DeletionTelomereThiones6-(4-hydroxyphenyl)-2-thioxo-2,3-dihydro-4(1H)-pyrimidinoneDNA-Binding ProteinsExodeoxyribonucleasesMRE11 Homologue ProteinMRE11 protein, humanPyrimidinonesThiones

Identifiers

PMID26209132
PMCPMC4652756
OpenAlexW1838003020

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.