ArticleGenes & development2014
Systematic screening reveals a role for BRCA1 in the response to transcription-associated DNA damage.
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Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
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77citing papers in PubMed, 1 pooled it
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Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci.Nucleic acids research · 2022Pooled it
- R-loop homeostasis at transposable elements safeguards transcriptional silencing in replication-quiescent oocytes.Nature communications · 2026Article
- Resolution of R-loops and transcription-replication conflicts by SETX-BRCA1-BARD1 complex.Nature structural & molecular biology · 2026Article
- BRCA1: An Unrecognized Modulator of Lineage Plasticity in Basal-like Breast Cancer.Journal of mammary gland biology and neoplasia · 2025Review
- Cancer histone mutations impact protein binding and DNA repair with possible links to genomic instability.Nucleic acids research · 2025Article
- Participants in Transcription-Replication Conflict and Their Role in Formation and Resolution of R-Loops.International journal of molecular sciences · 2025Review
- Update on R-loops in genomic integrity: Formation, functions, and implications for human diseases.Genes & diseases · 2025Review
- Breast cancer gene-1 (BRCA1) potentiates maladaptive repair after kidney injury.The Journal of experimental medicine · 2025Article
- BRCA1 and BRCA2: from cancer susceptibility to synthetic lethality.Genes & development · 2025Review
- R-loop functions inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- CWF19L2 is Essential for Male Fertility and Spermatogenesis by Regulating Alternative Splicing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Large tandem duplications in cancer result from transcription and DNA replication collisions.medRxiv : the preprint server for health sciences · 2024Article
- Role of senataxin in R-loop-mediated neurodegeneration.Brain communications · 2024Review
- RNF8 ubiquitylation of XRN2 facilitates R-loop resolution and restrains genomic instability in BRCA1 mutant cells.Nucleic acids research · 2023Article
- Senataxin and R-loops homeostasis: multifaced implications in carcinogenesis.Cell death discovery · 2023Review
- Emerging role for R-loop formation in hepatocellular carcinoma.Genes & genomics · 2023Review
- TONSL Is an Immortalizing Oncogene and a Therapeutic Target in Breast Cancer.Cancer research · 2023Article
- The BRCA1 BRCT promotes antisense RNA production and double-stranded RNA formation to suppress ribosomal R-loops.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- spKAS-seq reveals R-loop dynamics using low-input materials by detecting single-stranded DNA with strand specificity.Science advances · 2022Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 4 institutions in 2 countries.
Sarah J HillDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA;
Thomas RollandDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
Guillaume AdelmantDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA; Blais Proteomics Center, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
Xianfang XiaDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
Matthew S OwenDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
Amélie DricotDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
Travis I ZackDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; The Broad Institute, Cambridge, Massachusetts 02142, USA;
Nidhi SahniDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
Yves JacobDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Département de Virologie, Unité de Génétique Moléculaire des Virus à ARN, Institut Pasteur, F-75015 Paris, France; UMR3569, Centre National de la Recherche Scientifique, F-75015 Paris, France; Unité de Génétique Moléculaire des Virus à ARN, Université Paris Diderot, F-75015 Paris, France;
Tong HaoDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
Kristine M McKinneyDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA;
Allison P ClarkDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA;
Deepak ReyonMolecular Pathology Unit, Center for Computational and Integrative Biology, Center for Cancer Research, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA; Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA;
Shengdar Q TsaiMolecular Pathology Unit, Center for Computational and Integrative Biology, Center for Cancer Research, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA; Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA;
J Keith JoungMolecular Pathology Unit, Center for Computational and Integrative Biology, Center for Cancer Research, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA; Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA;
Rameen BeroukhimDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; The Broad Institute, Cambridge, Massachusetts 02142, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA.
Jarrod A MartoDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA; Blais Proteomics Center, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
Marc VidalDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
Suzanne GaudetDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
David E HillDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; Center for Cancer Systems Biology (CCSB), Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;
David M LivingstonDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA; david_livingston@dfci.harvard.edu.
Dana-Farber Cancer Institute · USHarvard University · USBroad Institute · USCenter for Cancer Research · US
Funding
Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0MUse of Organotypic and Mammary Gland Models to Investigate the Outcomes of ClonalP01CA080111 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI DILLON, DEBORAH · 1999 to 2018
$36.0MVariation in Receptor Tyrosine Kinases and Breast Cancer RiskP50CA089393 · NCI · DANA-FARBER CANCER INSTITUTE · PI HARRIS, LYNDSAY NORINE · 2000 to 2009
$28.8MSignatures of Kinase Activation in Cancer (MIT consortium)U54CA112962 · NCI · DANA-FARBER CANCER INSTITUTE · PI GOLUB, TODD R. · 2004 to 2014
$24.2MThe C. elegans Interactome ProjectR01HG001715 · NHGRI · MASSACHUSETTS GENERAL HOSPITAL · PI HILL, DAVID E., ROTH, FREDERICK P · 1998 to 2010
$16.5MTranscriptional control of inhibitory synapse formationP01NS047572 · NINDS · DANA-FARBER CANCER INSTITUTE · PI STILES, CHARLES D · 2004 to 2013
$13.5MMapping the first half of the REFERENCE human binary protein interactomeU01HG001715 · NHGRI · DANA-FARBER CANCER INST · PI HILL, DAVID E., ROTH, FREDERICK P · 2012 to 2014
$5.4MBRCA1 Function in Post-Damage Nuclear FociR01CA136512 · NCI · DANA-FARBER CANCER INST · PI LIVINGSTON, DAVID MORSE · 2009 to 2019
$4.6MAdvancing stem cell technologies using engineered zinc finger proteinsDP1GM105378 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI JOUNG, J. KEITH · 2012 to 2014
$2.6MMolecular analysis of the function of BRCA1-TONSL complexesF30CA167895 · NCI · HARVARD MEDICAL SCHOOL · PI HILL, SARAH JAMES · 2012 to 2015
$181kNCCDPHP CDC HHS DP1 GM105378NCI NIH HHS 1F30CA167895-01NCI NIH HHS F30 CA167895NCI NIH HHS P01 CA080111NCI NIH HHS P01CA080111NCI NIH HHS P50 CA089393NCI NIH HHS P50CA089393NCI NIH HHS R01 CA136512NCI NIH HHS R01CA136512NCI NIH HHS U54 CA112962NCI NIH HHS U54CA112962NHGRI NIH HHS R01 HG001715NHGRI NIH HHS R01HG001715NIGMS NIH HHS DP1 GM105378NIGMS NIH HHS T32 GM007753NINDS NIH HHS P01 NS047572NINDS NIH HHS P01NS047572
Abstract
BRCA1 is a breast and ovarian tumor suppressor. Given its numerous incompletely understood functions and the possibility that more exist, we performed complementary systematic screens in search of new BRCA1 protein-interacting partners. New BRCA1 functions and/or a better understanding of existing ones were sought. Among the new interacting proteins identified, genetic interactions were detected between BRCA1 and four of the interactors: TONSL, SETX, TCEANC, and TCEA2. Genetic interactions were also detected between BRCA1 and certain interactors of TONSL, including both members of the FACT complex. From these results, a new BRCA1 function in the response to transcription-associated DNA damage was detected. Specifically, new roles for BRCA1 in the restart of transcription after UV damage and in preventing or repairing damage caused by stabilized R loops were identified. These roles are likely carried out together with some of the newly identified interactors. This new function may be important in BRCA1 tumor suppression, since the expression of several interactors, including some of the above-noted transcription proteins, is repeatedly aberrant in both breast and ovarian cancers.
Indexed as
BRCA1 ProteinCell Line, TumorDNA DamageDNA RepairHeLa CellsHumansNF-kappa BProtein BindingProtein Interaction MappingTranscription, GeneticUltraviolet RaysBRCA1 ProteinBRCA1 protein, humanNF-kappa BTONSL protein, humanBRCA1 interaction screeningDNA damagetranscription
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