Evidence map›Paper›PMID 7724535›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Loss of the catalytic subunit of the DNA-dependent protein kinase in DNA double-strand-break-repair mutant mammalian cells.

S R Peterson, A Kurimasa, M Oshimura, W S Dynan, E M Bradbury, D J Chen

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
16.5field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 285 citations in OpenAlex.

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  15. Determinates of tumor response to radiation: tumor cells, tumor stroma and permanent local control.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2014
    Article
  16. Inhibition of DNA double-strand break repair by the dual PI3K/mTOR inhibitor NVP-BEZ235 as a strategy for radiosensitization of glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Article
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  18. Oversized AAV transductifon is mediated via a DNA-PKcs-independent, Rad51C-dependent repair pathway.Molecular therapy : the journal of the American Society of Gene Therapy · 2013
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36 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

S R PetersonLife Sciences Division, Los Alamos National Laboratory, NM 87545, USA.
A Kurimasa
M Oshimura
W S Dynan
E M Bradbury
D J Chen
Los Alamos National Laboratory · US

Funding

Roles of DNA PK in DNA Double Strand Break RepairR37CA050519 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI CHEN, DAVID J · 2003 to 2011
$3.5M
MOLECULAR MECHANISM OF TRANSCRIPTIONAL ACTIVATIONR01GM035866 · NIGMS · UNIVERSITY OF COLORADO AT BOULDER · PI DYNAN, WILLIAM S · 1986 to 2004
$1.1M
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 CA50519NIGMS NIH HHS GM35866
6 · The paper itself

Abstract

The DNA-dependent protein kinase (DNA-PK) consists of three polypeptide components: Ku-70, Ku-80, and an approximately 350-kDa catalytic subunit (p350). The gene encoding the Ku-80 subunit is identical to the x-ray-sensitive group 5 complementing gene XRCC5. Expression of the Ku-80 cDNA rescues both DNA double-strand break (DSB) repair and V(D)J recombination in group 5 mutant cells. The involvement of Ku-80 in these processes suggests that the underlying defect in these mutant cells may be disruption of the DNA-PK holoenzyme. In this report we show that the p350 kinase subunit is deleted in cells derived from the severe combined immunodeficiency mouse and in the Chinese hamster ovary cell line V-3, both of which are defective in DSB repair and V(D)J recombination. A centromeric fragment of human chromosome 8 that complements the scid defect also restores p350 protein expression and rescues in vitro DNA-PK activity. These data suggest the scid gene may encode the p350 protein or regulate its expression and are consistent with a model whereby DNA-PK is a critical component of the DSB-repair pathway.

Indexed as

Antigens, NuclearDNA HelicasesAnimalsCHO CellsCricetinaeDNA-Activated Protein KinaseDNA-Binding ProteinsDNA RepairFluorescent Antibody TechniqueKu AutoantigenMiceMice, SCIDNuclear ProteinsProtein Serine-Threonine KinasesRecombination, GeneticSevere Combined ImmunodeficiencyAntigens, NuclearDNA-Activated Protein KinaseDNA-Binding ProteinsDNA HelicasesKu AutoantigenNuclear ProteinsProtein Serine-Threonine KinasesXRCC5 protein, humanXrcc5 protein, mouseXrcc6 protein, humanXrcc6 protein, mouse

Identifiers

PMID7724535
PMCPMC42127
OpenAlexW2084957288

What OpenQuestion holds

Textmetadata
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.