Evidence map›Paper›PMID 20670897›Full record

ArticleMolecular cell2010

The terminal telomeric DNA sequence determines the mechanism of dysfunctional telomere fusion.

Bradley A Stohr, Lifeng Xu, Elizabeth H Blackburn

Abstract read
In one paragraph

Article in Molecular cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. How RNAi machinery enters the world of telomerase.Cell cycle (Georgetown, Tex.) · 2019
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. A self-regulating template in human telomerase.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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.

Bradley A StohrDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Lifeng Xu
Elizabeth H Blackburn

Funding

Tissue and Outcomes CoreP50CA058207 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRAY, JOE W. · 1992 to 2012
$32.7M
Synergism of telomere maintenance and telomerase with cancer-promoting signalingR01CA096840 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BLACKBURN, ELIZABETH H · 2002 to 2016
$4.8M
The Response of Cancer and Stem/Progenitor Cells to Telomere DisruptionK08CA134552 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STOHR, BRADLEY · 2009 to 2013
$753k
TUMOR CELL MEMBRANE MOLECULE INDUCTION OF MONOCYTE TNFR01CA058205 · NCI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI HALL, ROBERT E · 1992 to 1994
–
NCI NIH HHS CA58205NCI NIH HHS K08 CA134552NCI NIH HHS P50 CA058207NCI NIH HHS R01 CA096840
6 · The paper itself

Abstract

Mammalian telomeres consist of tandem DNA repeats that bind protective protein factors collectively termed shelterins. Telomere disruption typically results in genome instability induced by telomere fusions. The mechanism of telomere fusion varies depending on the means of telomere disruption. Here, we investigate telomere fusions caused by overexpression of mutant telomerases that add mutated telomeric repeats, thereby compromising shelterin binding to telomeric termini. While all mutant telomeric sequences tested induced heterodicentric chromosome fusions in ATM-competent cells, only those mutant repeat sequences with significant self complementarity induced ATM-independent sister chromatid and isodicentric chromosome fusions. Thus, once a telomere becomes dysfunctional, the terminal telomeric sequence itself determines the fate of that telomere. These results suggest that annealing of self-complementary DNA sequence engages an alternative telomere fusion pathway in human cells, and provide one explanation for the conspicuous lack of self complementarity in the majority of known naturally occurring eukaryotic telomeric sequences.

Indexed as

Genomic InstabilityTandem Repeat SequencesAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TumorChromatidsChromosomes, HumanDNA-Binding ProteinsHumansMutationProtein Serine-Threonine KinasesTelomeraseTelomereTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Binding ProteinsProtein Serine-Threonine KinasesTelomeraseTumor Suppressor Proteins

Identifiers

PMID20670897
PMCPMC2920734

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Registered trials

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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.