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http://hdl.handle.net/2445/124353
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DC Field | Value | Language |
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dc.contributor.author | Zhang, Xiaowen | - |
dc.contributor.author | Chiang, Huai-Chin | - |
dc.contributor.author | Wang, Yao | - |
dc.contributor.author | Zhang, Chi | - |
dc.contributor.author | Smith, Sabrina | - |
dc.contributor.author | Zhao, Xiayan | - |
dc.contributor.author | Nair, Sreejith J. | - |
dc.contributor.author | Michalek, Joel | - |
dc.contributor.author | Jatoi, Ismail | - |
dc.contributor.author | Lautner, Meeghan | - |
dc.contributor.author | Oliver, Boyce | - |
dc.contributor.author | Wang, Howard | - |
dc.contributor.author | Petit, Anna | - |
dc.contributor.author | Soler, María Teresa | - |
dc.contributor.author | Brunet, Joan | - |
dc.contributor.author | Mateo González, Francesca | - |
dc.contributor.author | Pujana Genestar, M. Ángel | - |
dc.contributor.author | Poggi, Elizabeth | - |
dc.contributor.author | Chaldekas, Krysta | - |
dc.contributor.author | Isaacs, Claudine | - |
dc.contributor.author | Peshkin, Beth N. | - |
dc.contributor.author | Ochoa, Oscar | - |
dc.contributor.author | Chedin, Frederic | - |
dc.contributor.author | Theoharis, Constantine | - |
dc.contributor.author | Sun, Lu-Zhe | - |
dc.contributor.author | Curiel, Tyler J. | - |
dc.contributor.author | Elledge, Richard | - |
dc.contributor.author | Jin, Victor X. | - |
dc.contributor.author | Hu, Yanfen | - |
dc.contributor.author | Li, Rong | - |
dc.date.accessioned | 2018-09-06T08:30:16Z | - |
dc.date.available | 2018-09-06T08:30:16Z | - |
dc.date.issued | 2017-06-26 | - |
dc.identifier.uri | http://hdl.handle.net/2445/124353 | - |
dc.description.abstract | Most BRCA1-associated breast tumours are basal-like yet originate from luminal progenitors. BRCA1 is best known for its functions in double-strand break repair and resolution of DNA replication stress. However, it is unclear whether loss of these ubiquitously important functions fully explains the cell lineage-specific tumorigenesis. In vitro studies implicate BRCA1 in elimination of R-loops, DNA-RNA hybrid structures involved in transcription and genetic instability. Here we show that R-loops accumulate preferentially in breast luminal epithelial cells, not in basal epithelial or stromal cells, of BRCA1 mutation carriers. Furthermore, R-loops are enriched at the 50 end of those genes with promoter-proximal RNA polymerase II (Pol II) pausing. Genetic ablation of Cobra1, which encodes a Pol II-pausing and BRCA1-binding protein, ameliorates R-loop accumulation and reduces tumorigenesis in Brca1-knockout mouse mammary epithelium. Our studies show that Pol II pausing is an important contributor to BRCA1-associated R-loop accumulation and breast cancer development. | - |
dc.format.extent | 12 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Nature Publishing | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.1038/ncomms15908 | - |
dc.relation.ispartof | Nature Communications, 2017, vol. 8 | - |
dc.relation.uri | https://doi.org/10.1038/ncomms15908 | - |
dc.rights | cc by (c) Zhang et al., 2017 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | - |
dc.source | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) | - |
dc.subject.classification | Càncer de mama | - |
dc.subject.other | Breast cancer | - |
dc.title | Attenuation of RNA polymerase II pausing mitigates BRCA1-associated R-loop accumulation and tumorigenesis | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.date.updated | 2018-07-24T12:05:44Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 28649985 | - |
Appears in Collections: | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
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File | Description | Size | Format | |
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ZhangXW.pdf | 1.64 MB | Adobe PDF | View/Open |
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