Evidence map›Paper›PMID 21773671›Full record

ArticleCellular and molecular life sciences : CMLS2012

Rad51 and DNA-PKcs are involved in the generation of specific telomere aberrations induced by the quadruplex ligand 360A that impair mitotic cell progression and lead to cell death.

Laurent R Gauthier, Christine Granotier, Françoise Hoffschir, Olivier Etienne, Ali Ayouaz, Chantal Desmaze, Patrick Mailliet, Denis S Biard, François D Boussin

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. The Relevance of G-Quadruplexes for DNA Repair.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. G-Quadruplexes at Telomeres: Friend or Foe?Molecules (Basel, Switzerland) · 2020
    Review
  13. Fundamentals of G-quadruplex biology.Annual reports in medicinal chemistry · 2020
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. 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

9 authors at 5 institutions in 1 country.

Laurent R GauthierLaboratoire de Radiopathologie, Institut de Radiobiologie Cellulaire et Moléculaire, CEA, 18 route du Panorama, BP6, 92265, Fontenay-aux-Roses, France.
Christine Granotier
Françoise Hoffschir
Olivier Etienne
Ali Ayouaz
Chantal Desmaze
Patrick Mailliet
Denis S Biard
François D Boussin
Inserm · FRCEA Paris-Saclay - Etablissement de Fontenay-aux-roses · FRInstitut de Radiobiologie Cellulaire et Moléculaire · FRSanofi (France) · FRUniversité Paris-Saclay · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Functional telomeres are protected from non-homologous end-joining (NHEJ) and homologous recombination (HR) DNA repair pathways. Replication is a critical period for telomeres because of the requirement for reconstitution of functional protected telomere conformations, a process that involves DNA repair proteins. Using knockdown of DNA-PKcs and Rad51 expression in three different cell lines, we demonstrate the respective involvement of NHEJ and HR in the formation of telomere aberrations induced by the G-quadruplex ligand 360A during or after replication. HR contributed to specific chromatid-type aberrations (telomere losses and doublets) affecting the lagging strand telomeres, whereas DNA-PKcs-dependent NHEJ was responsible for sister telomere fusions as a direct consequence of G-quadruplex formation and/or stabilization induced by 360A on parental telomere G strands. NHEJ and HR activation at telomeres altered mitotic progression in treated cells. In particular, NHEJ-mediated sister telomere fusions were associated with altered metaphase-anaphase transition and anaphase bridges and resulted in cell death during mitosis or early G1. Collectively, these data elucidate specific molecular and cellular mechanisms triggered by telomere targeting by the G-quadruplex ligand 360A, leading to cancer cell death.

Indexed as

ApoptosisG-QuadruplexesTelomereAnaphaseCell LineDNA-Activated Protein KinaseDNA End-Joining RepairHomologous RecombinationHumansLigandsMetaphaseMitosisNuclear ProteinsPyridinesQuinolinesRad51 Recombinase2,6-N,N'-methyl-quinolinio-3-yl-pyridine dicarboxamideDNA-Activated Protein KinaseLigandsNuclear ProteinsPRKDC protein, humanPyridinesQuinolinesRad51 RecombinaseRNA, Small Interfering

Identifiers

PMID21773671
PMCPMC3265728
OpenAlexW2044536320

What OpenQuestion holds

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LicenceCC BY-NC
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.