Evidence map›Paper›PMID 22013166›Full record

ArticleNucleic acids research2012

RECQL5 cooperates with Topoisomerase II alpha in DNA decatenation and cell cycle progression.

Mahesh Ramamoorthy, Takashi Tadokoro, Ivana Rybanska, Avik K Ghosh, Robert Wersto, Alfred May, Tomasz Kulikowicz, Peter Sykora, Deborah L Croteau, Vilhelm A Bohr

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. DNA strand breaks at centromeres: Friend or foe?Seminars in cell & developmental biology · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. RECQL5 at theFrontiers in cell and developmental biology · 2020
    Review
  8. Review
  9. Article
  10. Review
  11. Topoisomerases as anticancer targets.The Biochemical journal · 2018
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. 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

10 authors at 2 institutions in 1 country.

Mahesh RamamoorthyLaboratory of Molecular Gerontology, Biomedical Research Center, 251 Bayview Boulevard, National Institute on Aging, NIH, Baltimore, MD 21224, USA.
Takashi Tadokoro
Ivana Rybanska
Avik K Ghosh
Robert Wersto
Alfred May
Tomasz Kulikowicz
Peter Sykora
Deborah L Croteau
Vilhelm A Bohr
Baltimore City Health Department · USNational Institute on Aging · US

Funding

Function of RecQ helicases in genome stabilityZIAAG000726 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$13.1M
Flow Cytometry Laboratory (Scientific Core)ZICAG000618 · NIA · NATIONAL INSTITUTE ON AGING · PI WENG, NAN-PING PETER · 2009 to 2025
$9.5M
Function of RecQ helicases in genome stabilityZ01AG000726 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1993 to 2008
$2.9M
Intramural NIH HHSNIA NIH HHS Z01-AG000726-18
6 · The paper itself

Abstract

DNA decatenation mediated by Topoisomerase II is required to separate the interlinked sister chromatids post-replication. SGS1, a yeast homolog of the human RecQ family of helicases interacts with Topoisomerase II and plays a role in chromosome segregation, but this functional interaction has yet to be identified in higher organisms. Here, we report a physical and functional interaction of Topoisomerase IIα with RECQL5, one of five mammalian RecQ helicases, during DNA replication. Direct interaction of RECQL5 with Topoisomerase IIα stimulates the decatenation activity of Topoisomerase IIα. Consistent with these observations, RECQL5 co-localizes with Topoisomerase IIα during S-phase of the cell cycle. Moreover, cells with stable depletions of RECQL5 display a slow proliferation rate, a G2/M cell cycle arrest and late S-phase cycling defects. Metaphase spreads generated from RECQL5-depleted cells exhibit undercondensed and entangled chromosomes. Further, RECQL5-depleted cells activate a G2/M checkpoint and undergo apoptosis. These phenotypes are similar to those observed when Topoisomerase II catalytic activity is inhibited. These results reveal an important role for RECQL5 in the maintenance of genomic stability and a new insight into the decatenation process.

Indexed as

Cell CycleAntigens, NeoplasmApoptosisCell Cycle CheckpointsCell LineCell ProliferationChromosome AberrationsDNA-Binding ProteinsDNA, CatenatedDNA Topoisomerases, Type IIExodeoxyribonucleasesHumansMetaphaseRecQ HelicasesWerner Syndrome HelicaseAntigens, NeoplasmDNA-Binding ProteinsDNA, CatenatedDNA Topoisomerases, Type IIExodeoxyribonucleasesRecQ HelicasesRECQL5 protein, humanWerner Syndrome HelicaseWRN protein, human

Identifiers

PMID22013166
PMCPMC3287182
OpenAlexW2155120713

What OpenQuestion holds

Textmetadata
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.