| http://purl.uniprot.org/citations/21409565 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21409565 | http://www.w3.org/2000/01/rdf-schema#comment | "EMSY links the BRCA2 pathway to sporadic breast/ovarian cancer. It encodes a nuclear protein that binds to the BRCA2 N-terminal domain implicated in chromatin/transcription regulation, but when sporadically amplified/overexpressed, increased EMSY level represses BRCA2 transactivation potential and induces chromosomal instability, mimicking the activity of BRCA2 mutations in the development of hereditary breast/ovarian cancer. In addition to chromatin/transcription regulation, EMSY may also play a role in the DNA-damage response, suggested by its ability to localize at chromatin sites of DNA damage/repair. This implies that EMSY overexpression may also repress BRCA2 in DNA-damage replication/checkpoint and recombination/repair, coordinated processes that also require its interacting proteins: PALB2, the partner and localizer of BRCA2; RPA, replication/checkpoint protein A; and RAD51, the inseparable recombination/repair enzyme. Here, using a well-characterized recombination/repair assay system, we demonstrate that a slight increase in EMSY level can indeed repress these two processes independently of transcriptional interference/repression. Since EMSY, RPA and PALB2 all bind to the same BRCA2 region, these findings further support a scenario wherein: (a) EMSY amplification may mimic BRCA2 deficiency, at least by overriding RPA and PALB2, crippling the BRCA2/RAD51 complex at DNA-damage and replication/transcription sites; and (b) BRCA2/RAD51 may coordinate these processes by employing at least EMSY, PALB2 and RPA. We extensively discuss the molecular details of how this can happen to ascertain its implications for a novel recombination mechanism apparently conceived as checkpoint rather than a DNA repair system for cell division, survival, death, and human diseases, including the tissue specificity of cancer predisposition, which may renew our thinking about targeted therapy and prevention."xsd:string |
| http://purl.uniprot.org/citations/21409565 | http://purl.org/dc/terms/identifier | "doi:10.1007/s00438-011-0612-5"xsd:string |
| http://purl.uniprot.org/citations/21409565 | http://purl.uniprot.org/core/author | "Belmaaza A."xsd:string |
| http://purl.uniprot.org/citations/21409565 | http://purl.uniprot.org/core/author | "Cousineau I."xsd:string |
| http://purl.uniprot.org/citations/21409565 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21409565 | http://purl.uniprot.org/core/name | "Mol Genet Genomics"xsd:string |
| http://purl.uniprot.org/citations/21409565 | http://purl.uniprot.org/core/pages | "325-340"xsd:string |
| http://purl.uniprot.org/citations/21409565 | http://purl.uniprot.org/core/title | "EMSY overexpression disrupts the BRCA2/RAD51 pathway in the DNA-damage response: implications for chromosomal instability/recombination syndromes as checkpoint diseases."xsd:string |
| http://purl.uniprot.org/citations/21409565 | http://purl.uniprot.org/core/volume | "285"xsd:string |
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