http://rdf.ncbi.nlm.nih.gov/pubchem/patent/EP-1025203-A1
Outgoing Links
| Predicate | Object |
|---|---|
| assignee | http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_a4546b47ff59fa8318a14f80a9a0d071 |
| classificationCPCAdditional | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2217-05 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2217-075 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2227-105 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2267-0331 |
| classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12N15-8509 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K14-4703 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K67-0275 |
| classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12N5-10 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07K14-47 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12N15-85 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12N15-09 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/G01N33-50 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/G01N33-15 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A01K67-027 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12Q1-68 |
| filingDate | 1998-08-25-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor | http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_4a4423cf41bbe1e8dff6e64403e3f38a http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_d62d5c0d6763cd3e7c4fc67aa64e5e24 |
| publicationDate | 2000-08-09-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber | EP-1025203-A1 |
| titleOfInvention | Impaired brca2 function in cells and non-human transgenic animals |
| abstract | ScRad51, a member of the RAD52 epistasis group in Saccharomyces cerevisiae, is a major component in the recombinational repair pathway employed to repair genetic damage caused by ionizing radiation. The mouse homologue of ScRad51, MmRad51, appears to have a similar function; however, the precise mechanism of action is not well understood. For ScRad51, protein:protein associations are critical for function. Therefore, the yeast two-hybrid system was used to isolate proteins that associate with MmRad51 to better understand recombinational repair in mammalian cells and mouse Brca2 was isolated. In humans, BRCA2, is a tumor suppressor gene important in the etiology of breast cancer. A phenotypic comparison between MmRad51 and Brca2-deficient embryos and cells suggest the protein:protein association is important for their function. Similar to MmRad51, Brca2 function is critical for repair of gamma -radiation induced damage. In addition, a subtle mutation that removes only the small portion of Brca2 that associates with MmRad51, either directly or indirectly, exhibited a phenotype that suggests partial function. These homozygous mutant cells are viable yet hypersensitive to ionizing radiation and undergo premature replicative senescence. Cells and mice were generated with impaired Brca2 function that should prove useful as a model for tumorigenesis, a model to analyze genotoxic agents and as a tool to study premature replicative senescence. |
| priorityDate | 1997-08-26-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type | http://data.epo.org/linked-data/def/patent/Publication |
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