http://rdf.ncbi.nlm.nih.gov/pubchem/patent/KR-20140018478-A
Outgoing Links
| Predicate | Object |
|---|---|
| assignee | http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_2b4be2300a741a69aa1b8bb47a88899f |
| classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K39-395 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-4745 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K48-00 |
| classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61P31-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-7105 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-7088 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K48-00 |
| filingDate | 2012-07-31-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor | http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_361d962a0f8878ec71f4576c056be842 http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_2df335f7df7e8ebe80dba084631a2264 |
| publicationDate | 2014-02-13-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber | KR-20140018478-A |
| titleOfInvention | Hepatitis C prophylaxis and treatment composition comprising a cyclin A2 inhibitor |
| abstract | Background and Purpose : Hepatitis C virus (HCV) requires host cell proteins for proliferation. To identify the cell factors essential for HCV proliferation, siRNA libraries targeting cell cycles were screened using HCV infected cells grown in cell proliferation, and genes encoding cyclin A2 were selected and characterized. CycA2 deregulation has been associated with several types of tumors, including liver cancer. Methods : The effect of CycA2 on HCV proliferation was studied by siRNA mediated knockdown assay, in vitro and in vivo protein binding assay, luciferase reporter gene assay and immunoblotting assay. RESULTS : siRNA-mediated CycA2 reduction significantly inhibited HCV replication in both HCV subgenomic replicon cells and HCVcc infected cells. In addition, HCV NS5B specifically interacted with CycA2 in vitro and in vivo. Protein interactions were mediated through the cyclin box of CycA2 and the palm domain of NS5B. The R / HxL motif of the palm domain of HCV NS5B mediates protein interactions with CycA2, which is essential for HCV replication. Furthermore, tyloporin, a product of natural plants with CycA2 inhibitory function, inhibited HCV replication. CONCLUSIONS: HCV modulates CycA2 through NS5B protein for self proliferation, and tyloporin has potential as a therapeutic agent for HCV. |
| priorityDate | 2012-07-31-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type | http://data.epo.org/linked-data/def/patent/Publication |
Incoming Links
Total number of triples: 438.