Evidence map›Paper›PMID 22265216›Full record

ArticleDNA repair2012

Persistently bound Ku at DNA ends attenuates DNA end resection and homologous recombination.

Zhengping Shao, Anthony J Davis, Kazi R Fattah, Sairei So, Jingxin Sun, Kyung-Jong Lee, Lynn Harrison, Jun Yang, David J Chen

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
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  18. Article
  19. The Multifaceted Roles of Ku70/80.International journal of molecular sciences · 2021
    Review
  20. MonitoringBiology open · 2021
    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 3 institutions in 2 countries.

Zhengping ShaoDivision of Molecular Radiation Biology, Department of Radiation Oncology, The University of Texas Southwestern Medical Center, 2201 Inwood Rd, Dallas, TX 75390, USA.
Anthony J Davis
Kazi R Fattah
Sairei So
Jingxin Sun
Kyung-Jong Lee
Lynn Harrison
Jun Yang
David J Chen
The University of Texas Southwestern Medical Center · USZhejiang University · CNLouisiana State University Health Sciences Center New Orleans · US

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI John A. Tainer · 2001 to 2026
$89.6M
Roles of DNA PK in DNA Double Strand Break RepairR37CA050519 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI CHEN, DAVID J · 2003 to 2011
$3.5M
Pathway Choice of DNA Double-Strand Break RepairR01CA162804 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI DAVIS, ANTHONY J · 2012 to 2021
$3.4M
DNA REPAIR OF MULTIPLY DAMAGED SITES IN CELLSR01CA085693 · NCI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI HARRISON, LYNN · 2000 to 2010
$2.4M
Functions of WRN in Response to DNA Double-Strand BreaksR01CA134991 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI CHEN, DAVID J · 2009 to 2013
$1.6M
ROLES OF DNA PK IN DNA DOUBLE STRAND BREAK REPAIRR01CA050519 · NCI · UNIVERSITY OF CALIF-LOS ALAMOS NAT LAB · PI CHEN, DAVID J · 1989 to 2001
$946k
NCI NIH HHS CA134991NCI NIH HHS CA50519NCI NIH HHS CA85693NCI NIH HHS CA85693-9S1NCI NIH HHS CA92584NCI NIH HHS P01 CA092584NCI NIH HHS R01 CA050519NCI NIH HHS R01 CA085693NCI NIH HHS R01 CA134991NCI NIH HHS R01 CA162804NCI NIH HHS R37 CA050519
6 · The paper itself

Abstract

DNA double strand breaks (DSBs) are repaired by non-homologous end joining (NHEJ) or homologous recombination (HR). The DNA cell cycle stage and resection of the DSB ends are two key mechanisms which are believed to push DSB repair to the HR pathway. Here, we show that the NHEJ factor Ku80 associates with DSBs in S phase, when HR is thought to be the preferred repair pathway, and its dynamics/kinetics at DSBs is similar to those observed for Ku80 in non-S phase in mammalian cells. A Ku homolog from Mycobacterium tuberculosis binds to and is retained at DSBs in S phase and was used as a tool to determine if blocking DNA ends affects end resection and HR in mammalian cells. A decrease in DNA end resection, as marked by IR-induced RPA, BrdU, and Rad51 focus formation, and HR are observed when Ku deficient rodent cells are complemented with Mt-Ku. Together, this data suggests that Ku70/80 binds to DSBs in all cell cycle stages and is likely actively displaced from DSB ends to free the DNA ends for DNA end resection and thus HR to occur.

Indexed as

DNA Breaks, Double-StrandedAnimalsAntigens, NuclearCHO CellsCricetinaeCricetulusDNADNA-Binding ProteinsDNA RepairHomologous RecombinationHumansKu AutoantigenMiceMycobacterium tuberculosisProtein BindingProtein TransportAntigens, NuclearDNADNA-Binding ProteinsKu AutoantigenRad51 RecombinaseXrcc6 protein, humanXrcc6 protein, mouse

Identifiers

PMID22265216
PMCPMC3297478
OpenAlexW2012882202

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.