http://rdf.ncbi.nlm.nih.gov/pubchem/patent/KR-100746585-B1
Outgoing Links
Predicate | Object |
---|---|
classificationCPCAdditional | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2267-0318 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2217-072 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2227-105 |
classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K67-0275 |
classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A01K67-027 |
filingDate | 2004-05-17-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
grantDate | 2007-08-08-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
publicationDate | 2007-08-08-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
publicationNumber | KR-100746585-B1 |
titleOfInvention | How to treat motility disorders by modulating the α1-T-type channel gene targeting mice with increased stimulation-type personality and alcohol preference |
abstract | The present invention relates to a novel use as a neurological disease model in α1G T-type calcium channel mutant mice, in particular the α1G T-type calcium channel, which exhibits a novel stimulation-seeking and alcohol preference, is deficient. And use of a mouse as a model of neurological disorders associated with emotional and anorexic disorders such as stimulus-purifying personality disorder, alcoholism and stress in humans. The novel stimulus seeking and alcohol preference of the α1G T-type calcium channel mutant mice of the present invention may be usefully used in the development of drugs and therapeutic methods for human neurological diseases. |
priorityDate | 2004-05-04-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
type | http://data.epo.org/linked-data/def/patent/Publication |
Incoming Links
Total number of triples: 348.