Evidence map›Paper›PMID 20185827›Full record

ArticleThe Journal of biological chemistry2010

Transcriptional regulation of the base excision repair pathway by BRCA1.

Tapas Saha, Jeong Keun Rih, Rabindra Roy, Rahul Ballal, Eliot M Rosen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 87 citations in OpenAlex.

  1. Trial
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  3. Novel De NovoInternational journal of molecular sciences · 2025
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  10. An Excimer Clamp for Measuring Damaged-Base Excision by the DNA Repair Enzyme NTH1.Angewandte Chemie (International ed. in English) · 2020
    Article
  11. Review
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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.

Tapas SahaDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA.
Jeong Keun Rih
Rabindra Roy
Rahul Ballal
Eliot M Rosen
Georgetown University · USGeorgetown University Medical Center · US

Funding

Regulations of DNA Alkylation/Deamination Damage RepairR01CA092306 · NCI · INSTITUTE FOR CANCER PREVENTION · PI ROY, RABINDRA · 2003 to 2013
$2.8M
BRCA1 Modulates Estrogen Receptor Response in CancerR01CA082599 · NCI · LONG ISLAND JEWISH MEDICAL CENTER · PI ROSEN, ELIOT M. · 1999 to 2009
$2.2M
Role of BRCA1 as a Human Tumor Suppressor GeneR01CA080000 · NCI · LONG ISLAND JEWISH MEDICAL CENTER · PI ROSEN, ELIOT M. · 1999 to 2008
$1.6M
BRCA Genes in Breast Cancer ChemopreventionR01CA104546 · NCI · GEORGETOWN UNIVERSITY · PI ROSEN, ELIOT M. · 2005 to 2009
$1.5M
NCI NIH HHS R01 CA080000NCI NIH HHS R01 CA082599NCI NIH HHS R01 CA092306NCI NIH HHS R01 CA104546NCI NIH HHS R01-CA104546NCI NIH HHS R01-CA80000NCI NIH HHS R01-CA82599
6 · The paper itself

Abstract

Inactivation of the breast cancer susceptibility gene BRCA1 plays a significant role in the development of a subset of breast cancers, although the major tumor suppressor function of this gene remains unclear. Previously, we showed that BRCA1 induces antioxidant-response gene expression and protects cells against oxidative stress. We now report that BRCA1 stimulates the base excision repair pathway, a major mechanism for the repair of oxidized DNA, by stimulating the activity of key base excision repair (BER) enzymes, including 8-oxoguanine DNA glycosylase (OGG1), the DNA glycosylase NTH1, and the apurinic endonuclease redox factor 1/apurinic endonuclease 1 (REF1/APE1), in human breast carcinoma cells. The increase in BER enzyme activity appears to be due, primarily, to an increase in enzyme expression. The ability of BRCA1 to stimulate the expression of the three BER enzymes and to enhance NTH1 promoter activity was dependent upon the octamer-binding transcription factor OCT1. Finally, we found that OGG1, NTH1, and REF1/APE1 each contribute to the BRCA1 protection against oxidative stress due to hydrogen peroxide and that hydrogen peroxide stimulates the expression of BRCA1 and the three BER enzymes. These findings identify a novel mechanism through which BRCA1 may regulate the repair of oxidative DNA damage.

Indexed as

DNA RepairGene Expression Regulation, NeoplasticTranscription, GeneticAnimalsBRCA1 ProteinCell Line, TumorDNA DamageDNA GlycosylasesFibroblastsHumansHydrogen PeroxideMiceOxidative StressRNA, Small InterferingTranscription FactorsBRCA1 ProteinBRCA1 protein, humanDNA GlycosylasesHydrogen Peroxideoxoguanine glycosylase 1, humanRNA, Small InterferingTranscription Factors

Identifiers

PMID20185827
PMCPMC2885188
OpenAlexW1994025613

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.