Evidence map›Paper›PMID 16522646›Full record

ArticleNucleic acids research2006

Repression of mutagenesis by Rad51D-mediated homologous recombination.

John M Hinz, Robert S Tebbs, Paul F Wilson, Peter B Nham, Edmund P Salazar, Hatsumi Nagasawa, Salustra S Urbin, Joel S Bedford, Larry H Thompson

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.4field-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

45 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
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  14. The Effect of Green and Black Tea Polyphenols onInternational journal of molecular sciences · 2019
    Article
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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 1 institution in 1 country.

John M HinzBiosciences Directorate, Lawrence Livermore National Laboratory, Livermore, CA 94551, USA.
Robert S Tebbs
Paul F Wilson
Peter B Nham
Edmund P Salazar
Hatsumi Nagasawa
Salustra S Urbin
Joel S Bedford
Larry H Thompson
Lawrence Livermore National Laboratory · US

Funding

FANCONI ANEMIA GENE PATHWAY IN RADIATION RESPONSESR01CA089405 · NCI · UNIVERSITY OF CALIF-LAWRNC LVRMR NAT LAB · PI THOMPSON, LAWRENCE H · 2001 to 2004
$1.5M
Homologous Recombination & Human Cell RadiosensitivityR01CA112566 · NCI · UNIVERSITY OF CALIF-LAWRNC LVRMR NAT LAB · PI THOMPSON, LAWRENCE H · 2006 to 2009
$1.4M
NCI NIH HHS 1 R01 CA112566-01A1NCI NIH HHS CA89405NCI NIH HHS R01 CA089405NCI NIH HHS R01 CA112566
6 · The paper itself

Abstract

Homologous recombinational repair (HRR) restores chromatid breaks arising during DNA replication and prevents chromosomal rearrangements that can occur from the misrepair of such breaks. In vertebrates, five Rad51 paralogs are identified that contribute in a nonessential but critical manner to HRR proficiency. We constructed and characterized a knockout of the paralog Rad51D in widely studied CHO cells. The rad51d mutant (clone 51D1) displays sensitivity to a diverse spectrum of induced DNA damage including gamma-rays, ultraviolet (UV)-C radiation, and methyl methanesulfonate (MMS), indicating the broad relevance of HRR to genotoxicity. Spontaneous chromatid breaks/gaps and isochromatid breaks are elevated 3- to 12-fold, but the chromosome number distribution remains unchanged. Most importantly, 51D1 cells exhibit a 12-fold-increased rate of hprt mutation, as well as 4- to 10-fold increased rates of gene amplification at the dhfr and CAD loci, respectively. Xrcc3 irs1SF cells from the same parental CHO line show similarly elevated mutagenesis at these three loci. Collectively, these results confirm the a priori expectation that HRR acts in an error-free manner to repress three classes of genetic alterations (chromosomal aberrations, loss of gene function and increased gene expression), all of which are associated with carcinogenesis.

Indexed as

MutagenesisRecombination, GeneticAnimalsCell SurvivalCHO CellsChromosome AberrationsCricetinaeCricetulusDNA DamageGamma RaysGene AmplificationGene TargetingHypoxanthine PhosphoribosyltransferaseRad51 RecombinaseHypoxanthine PhosphoribosyltransferaseRad51 Recombinase

Identifiers

PMID16522646
PMCPMC1390685
OpenAlexW2036611623

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.