Evidence map›Paper›PMID 20226664›Full record

ArticleCurrent biology : CB2010

p53 prevents entry into mitosis with uncapped telomeres.

Maria Thanasoula, Jose Miguel Escandell, Paula Martinez, Sophie Badie, Purificacion Muñoz, María A Blasco, Madalena Tarsounas

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The Connection Between Cell Fate and Telomere.Advances in experimental medicine and biology · 2021
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. DNA damage to a single chromosome end delays anaphase onset.The Journal of biological chemistry · 2014
    Article
  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

7 authors at 2 institutions in 2 countries.

Maria ThanasoulaTelomere and Genome Stability Group, The CR-UK/MRC Gray Institute for Radiation Oncology and Biology, Old Road Campus, Oxford OX37DQ, UK.
Jose Miguel Escandell
Paula Martinez
Sophie Badie
Purificacion Muñoz
María A Blasco
Madalena Tarsounas
CRUK/MRC Oxford Institute for Radiation Oncology · GBSpanish National Cancer Research Centre · ES

Funding

Breast Cancer Now 2005NOV57Cancer Research UK A8935
6 · The paper itself

Abstract

Telomeres are protected by capping structures consisting of core protein complexes that bind with sequence specificity to telomeric DNA. In their absence, telomeres trigger a DNA damage response, materialized in accumulation at the telomere of damage response proteins, e.g., phosphorylated histone H2AX (gammaH2AX), into telomere-dysfunction-induced foci. Telomere uncapping occurs transiently in every cell cycle in G2, following DNA replication, but little is known about how protective structures are reassembled or whether this process is controlled by the cell-cycle surveillance machinery. Here, we report that telomere capping is monitored at the G2/M transition by the p53/p21 damage response pathway. Unlike their wild-type counterparts, human and mouse cells lacking p53 or p21 progress into mitosis prematurely with persisting uncapped telomeres. Furthermore, artificially uncapped telomeres delay mitotic entry in a p53- and p21-dependent manner. Uncapped telomeres that persist in mitotic p53-deficient cells are shorter than average and religate to generate end-to-end fusions. These results suggest that a p53-dependent pathway monitors telomere capping after DNA replication and delays G2/M progression in the presence of unprotected telomeres. This mechanism maintains a cell-cycle stage conducive for capping reactions and prevents progression into stages during which uncapped telomeres are prone to deleterious end fusions.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsBase SequenceCell Cycle ProteinsCell LineCells, CulturedCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsDNA DamageHeLa CellsHistonesHumansMiceMice, KnockoutMitosisProtein Serine-Threonine KinasesAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCDKN1A protein, humanCdkn1a protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21DNA-Binding Proteinsgamma-H2AX protein, mouseH2AX protein, humanHistonesProtein Serine-Threonine KinasesRNA, Small InterferingTP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID20226664
PMCPMC4959573
OpenAlexW2048228863

What OpenQuestion holds

Textmetadata
LicenceTDM
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.