Evidence map›Paper›PMID 18413737›Full record

ArticleCancer research2008

Distinct RAD51 associations with RAD52 and BCCIP in response to DNA damage and replication stress.

Justin Wray, Jingmei Liu, Jac A Nickoloff, Zhiyuan Shen

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

41 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  3. RAD52 prevents accumulation ofbioRxiv : the preprint server for biology · 2024
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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

4 authors at 2 institutions in 1 country.

Justin WrayDepartment of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Cancer Research and Treatment Center, Albuquerque, New Mexico, USA.
Jingmei Liu
Jac A Nickoloff
Zhiyuan Shen
Rutgers, The State University of New Jersey · USUniversity of New Mexico · US

Funding

MAMMILIAN DOUBLE STRAND BREAK AND RECOMBINATIONAL REPAIRR01CA077693 · NCI · UNIVERSITY OF NEW MEXICO · PI OSLEY, MARY ANN · 1999 to 2008
$2.4M
Protection of Genomic Integrity by BCCIPR01CA115488 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI SHEN, ZHIYUAN · 2005 to 2009
$1.3M
Transcription-enhanced recombination in mammalian cellsR01ES008353 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI SHEN, ZHIYUAN · 2003 to 2006
$1.0M
ROLES OF UBIQUITIN CONJUGATING ENZYMES IN DNA REPAIRR29ES008353 · NIEHS · UNIVERSITY OF NEW MEXICO · PI SHEN, ZHIYUAN · 1997 to 2001
$214k
NCI NIH HHS CA115488NCI NIH HHS CA77693NCI NIH HHS R01 CA077693NCI NIH HHS R01 CA115488NIEHS NIH HHS ES08353NIEHS NIH HHS R01 ES008353NIEHS NIH HHS R29 ES008353
6 · The paper itself

Abstract

RAD51 has critical roles in homologous recombination (HR) repair of DNA double-strand breaks (DSB) and restarting stalled or collapsed replication forks. In yeast, Rad51 function is facilitated by Rad52 and other "mediators." Mammalian cells express RAD52, but BRCA2 may have supplanted RAD52 in mediating RAD51 loading onto ssDNA. BCCIP interacts with BRCA2, and both proteins are important for RAD51 focus formation after ionizing radiation and HR repair of DSBs. Nonetheless, mammalian RAD52 shares biochemical activities with yeast Rad52, including RAD51 binding and single-strand annealing, suggesting a conserved role in HR. Because RAD52 and RAD51 associate, and RAD51 and BCCIP associate, we investigated the colocalization of RAD51 with BCCIP and RAD52 in human cells. We found that RAD51 colocalizes with BCCIP early after ionizing radiation, with RAD52 later, and there was little colocalization of BCCIP and RAD52. RAD52 foci are induced to a greater extent by hydroxyurea, which stalls replication forks, than by ionizing radiation. Using fluorescence recovery after photo bleaching, we show that RAD52 mobility is reduced to a greater extent by hydroxyurea than ionizing radiation. However, BCCIP showed no changes in mobility after hydroxyurea or ionizing radiation. We propose that BCCIP-dependent repair of DSBs by HR is an early RAD51 response to ionizing radiation-induced DNA damage, and that RAD52-dependent HR occurs later to restart a subset of blocked or collapsed replication forks. RAD52 and BRCA2 seem to act in parallel pathways, suggesting that targeting RAD52 in BRCA2-deficient tumors may be effective in treating these tumors.

Indexed as

DNA DamageDNA RepairRecombination, GeneticAntibodies, MonoclonalCalcium-Binding ProteinsCell Cycle ProteinsCell Line, TumorDNA ReplicationFibrosarcomaFluorescein-5-isothiocyanateGenes, ReporterHumansImmunohistochemistryLuciferasesNuclear ProteinsPlasmidsAntibodies, MonoclonalBCCIP protein, humanCalcium-Binding ProteinsCell Cycle ProteinsFluorescein-5-isothiocyanateLuciferasesNuclear ProteinsRAD51 protein, humanRad51 Recombinase

Identifiers

PMID18413737
PMCPMC2744103
OpenAlexW1987557338

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.