Evidence map›Paper›PMID 28549257›Full record

ArticleDNA repair2017

Human somatic cells deficient for RAD52 are impaired for viral integration and compromised for most aspects of homology-directed repair.

Yinan Kan, Nizar N Batada, Eric A Hendrickson

Abstract read
In one paragraph

Article in DNA repair, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

27 citing papers in PubMed, 31 citations in OpenAlex.

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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

3 authors at 2 institutions in 2 countries.

Yinan KanDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, Minneapolis, MN 55455, United States.
Nizar N BatadaDepartment of Medical Biophysics, University of Toronto, Toronto, Canada.
Eric A HendricksonBMBB Department, University of Minnesota Medical School, 6-155 Jackson Hall, 321 Church St., SE., Minneapolis, MN 55455, United States. Electronic address: hendr064@umn.edu.
University of Minnesota Medical Center · USUniversity of Toronto · CA

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Douglas Yee · 1998 to 2026
$100.4M
The mechanism of Cas9/CRISPR-initiated genome modification in human somatic cellsR01GM088351 · NIGMS · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2010 to 2018
$2.3M
Ligase III regulates survival from crisis induced by gradual telomere shorteningR01CA190492 · NCI · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2015 to 2019
$1.7M
Ku regulates non-homologous end joining pathways in human somatic cellsR01CA154461 · NCI · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2011 to 2015
$1.6M
NCI NIH HHS P30 CA077598NCI NIH HHS R01 CA154461NCI NIH HHS R01 CA190492NIGMS NIH HHS R01 GM088351
6 · The paper itself

Abstract

Homology-directed repair (HDR) maintains genomic integrity by eliminating lesions such as DNA double-strand breaks (DSBs), interstrand crosslinks (ICLs) and stalled replication forks and thus a deficiency in HDR is associated with genomic instability and cancer predisposition. The mechanism of HDR is best understood and most rigorously characterized in yeast. The inactivation of the fungal radiation sensitive 52 (RAD52) gene, which has both recombination mediator and single-strand annealing (SSA) activities in vitro, leads to severe HDR defects in vivo. Confusingly, however, the inactivation of murine and chicken RAD52 genes resulted in mouse and chicken cells, respectively, that were largely aphenotypic. To clarify this issue, we have generated RAD52 knockout human cell lines. Human RAD52-null cells retain a significant level of SSA activity demonstrating perforce that additional SSA-like activities must exist in human cells. Moreover, we confirmed that the SSA activity associated with RAD52 is involved in, but not absolutely required for, most HDR subpathways. Specifically, a deficiency in RAD52 impaired the repair of DNA DSBs and intriguingly decreased the random integration of recombinant adeno-associated virus (rAAV). Finally, an analysis of pan-cancer genome data from The Cancer Genome Atlas (TCGA) revealed an association between aberrant levels of RAD52 expression and poor overall survival in multiple cancers. In toto, our work demonstrates that RAD52 contributes to the maintenance of genome stability and tumor suppression in human cells.

Indexed as

DNA Breaks, Double-StrandedDNA RepairDNAGene Expression Regulation, NeoplasticGene Knockout TechniquesGenomic InstabilityHumansNeoplasmsRad52 DNA Repair and Recombination ProteinDNARad52 DNA Repair and Recombination ProteinRAD52 protein, humanDNA double-strand breaks (DSBs)Genome stabilityHomology-directed repair (HDR)Radiation sensitive 52 (RAD52)Single-strand annealing (SSA)

Identifiers

PMID28549257
PMCPMC5515278
OpenAlexW2613072143

What OpenQuestion holds

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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.