Evidence map›Paper›PMID 19667076›Full record

ArticleMolecular and cellular biology2009

The mre11 complex and the response to dysfunctional telomeres.

Claire L Attwooll, Müge Akpinar, John H J Petrini

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

49 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Telomeres in toxicology: Occupational health.Pharmacology & therapeutics · 2021
    Review
  13. Review
  14. Article
  15. 53BP1: a DSB escort.Genes & development · 2020
    Review
  16. Article
  17. MRE11 UFMylation promotes ATM activation.Nucleic acids research · 2019
    Article
  18. Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Claire L AttwoollLaboratory of Chromosome Biology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, RRL 901C Box 474, New York, NY 10021, USA.
Müge Akpinar
John H J Petrini
Memorial Sloan Kettering Cancer Center · US

Funding

ROLES OF MRELL AND RAD50 IN THE DNA DAMAGE RESPONSER01GM056888 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI PETRINI, JOHN HJ · 1998 to 2019
$8.6M
The Mre11 complex: linking recombination to checkpointsR01GM059413 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI PETRINI, JOHN HJ · 1999 to 2011
$5.2M
FASEB SRC on Genetic Recombination and Genome RearrangementsR13CA162528 · NCI · FEDERATION OF AMER SOC FOR EXPER BIOLOGY · PI PETRINI, JOHN HJ · 2011 to 2011
$5k
AGING, DISEASE, AND DRUGS ON DIGITALIS SENSITIVITYR01AG002398 · NIA · MICHIGAN STATE UNIVERSITY · PI BRODY, THEODORE M. · 1985 to 1988
–
NCI NIH HHS R13 CA162528NIA NIH HHS R01 AG02398NIGMS NIH HHS R01 GM056888NIGMS NIH HHS R01 GM059413
6 · The paper itself

Abstract

In this study, we examine the telomeric functions of the mammalian Mre11 complex by using hypomorphic Mre11 and Nbs1 mutants (Mre11(ATLD1/ATLD1) and Nbs1(Delta)(B/)(DeltaB), respectively). No telomere shortening was observed in Mre11(ATLD1/ATLD1) cells after extensive passage through culture, and the rate of telomere shortening in telomerase-deficient (Tert(Delta)(/)(Delta)) Mre11(ATLD1/ATLD1) cells was the same as that in Tert(Delta)(/)(Delta) alone. Although telomeres from late-passage Mre11(ATLD1/ATLD1) Tert(Delta)(/)(Delta) cells were as short as those from Tert(Delta)(/)(Delta), the incidence of telomere fusions was reduced. This effect on fusions was also evident upon acute telomere dysfunction in Mre11(ATLD1/ATLD1) and Nbs1(Delta)(B/)(DeltaB) cells rendered Trf2 deficient by cre-mediated TRF2 inactivation than in wild-type cells. The residual fusions formed in Mre11 complex mutant cells exhibited a strong tendency toward chromatid fusions, with an almost complete bias for fusion of telomeres replicated by the leading strand. Finally, the response to acute telomere dysfunction was strongly impaired by Mre11 complex hypomorphism, as the formation of telomere dysfunction-induced DNA damage foci was reduced in both cre-infected Mre11(ATLD1/ATLD1) Trf2(F/)(Delta) and Nbs1(Delta)(B/)(DeltaB) Trf2(F/F) cells. These data indicate that the Mre11 complex influences the cellular response to telomere dysfunction, reminiscent of its influence on the response to interstitial DNA breaks, and suggest that it may promote telomeric DNA end processing during DNA replication.

Indexed as

AnimalsCell Cycle ProteinsChromosomes, MammalianDNA-Binding ProteinsDNA DamageDNA Repair EnzymesFibroblastsMiceMRE11 Homologue ProteinNuclear ProteinsTelomereTelomeric Repeat Binding Protein 2Cell Cycle ProteinsDNA-Binding ProteinsDNA Repair EnzymesMre11a protein, mouseMRE11 Homologue ProteinNijmegen breakage syndrome 1 protein, mouseNuclear ProteinsTelomeric Repeat Binding Protein 2TRF2 protein, mouse

Identifiers

PMID19667076
PMCPMC2756889
OpenAlexW2110962554

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.