Evidence map›Paper›PMID 17947333›Full record

ArticleNucleic acids research2007

BCCIP regulates homologous recombination by distinct domains and suppresses spontaneous DNA damage.

Huimei Lu, Jingyin Yue, Xiangbing Meng, Jac A Nickoloff, Zhiyuan Shen

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

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  9. Roles of BCCIP deficiency in mammary tumorigenesis.Breast cancer research : BCR · 2017
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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

5 authors at 2 institutions in 1 country.

Huimei LuDepartment of Radiation Oncology, The Cancer Institute of New Jersey, UMDNJ-Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ 08903, USA.
Jingyin Yue
Xiangbing Meng
Jac A Nickoloff
Zhiyuan Shen
University of New Mexico · USRutgers Cancer Institute of New Jersey

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

Homologous recombination (HR) is critical for maintaining genome stability through precise repair of DNA double-strand breaks (DSBs) and restarting stalled or collapsed DNA replication forks. HR is regulated by many proteins through distinct mechanisms. Some proteins have direct enzymatic roles in HR reactions, while others act as accessory factors that regulate HR enzymatic activity or coordinate HR with other cellular processes such as the cell cycle. The breast cancer susceptibility gene BRCA2 encodes a critical accessory protein that interacts with the RAD51 recombinase and this interaction fluctuates during the cell cycle. We previously showed that a BRCA2- and p21-interacting protein, BCCIP, regulates BRCA2 and RAD51 nuclear focus formation, DSB-induced HR and cell cycle progression. However, it has not been clear whether BCCIP acts exclusively through BRCA2 to regulate HR and whether BCCIP also regulates the alternative DSB repair pathway, non-homologous end joining. In this study, we found that BCCIP fragments that interact with BRCA2 or with p21 each inhibit DSB repair by HR. We further show that transient down-regulation of BCCIP in human cells does not affect non-specific integration of transfected DNA, but significantly inhibits homology-directed gene targeting. Furthermore, human HT1080 cells with constitutive down-regulation of BCCIP display increased levels of spontaneous single-stranded DNA (ssDNA) and DSBs. These data indicate that multiple BCCIP domains are important for HR regulation, that BCCIP is unlikely to regulate non-homologous end joining, and that BCCIP plays a critical role in resolving spontaneous DNA damage.

Indexed as

DNA DamageRecombination, GeneticCalcium-Binding ProteinsCell Cycle ProteinsCell LineDNA Breaks, Double-StrandedDNA, Single-StrandedDown-RegulationGene TargetingHumansNuclear ProteinsProtein Structure, TertiaryBCCIP protein, humanCalcium-Binding ProteinsCell Cycle ProteinsDNA, Single-StrandedNuclear Proteins

Identifiers

PMID17947333
PMCPMC2175368
OpenAlexW2145246499

What OpenQuestion holds

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LicenceCC BY-NC
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.