Predicate |
Object |
assignee |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_036e1006f60df667be54d6f6b2bb8964 http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_05bea87a3092bdb31ddcf14ee93a7937 |
classificationIPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A01K67-027 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12N15-09 |
filingDate |
1996-07-23-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
inventor |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_053c39b2c565fc389597e80b18f8f721 http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_cb8f2a98b9898357e7def125ba2fc4a1 |
publicationDate |
1998-02-10-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
publicationNumber |
JP-H1033087-A |
titleOfInvention |
Glutamate transporter gene function deficient non-human animal |
abstract |
(57) [Summary] [Problem] To provide an experimental animal for studying pathophysiology and pathogenesis of neurodegenerative diseases and nerve cell death involving glutamate, elucidation of etiology, development of treatment methods, and the like. SOLUTION: The function of an animal glutamate transporter gene is deleted. In particular, GluT-1 gene and / or Glutamate transporter gene The function of the LT1 gene is deleted in the chromosomes of somatic cells and germ cells to generate knockout animals. |
isCitedBy |
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/JP-WO2004092371-A1 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/JP-2006526634-A http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-7642399-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/JP-4494340-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2004092371-A1 |
priorityDate |
1996-07-23-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
type |
http://data.epo.org/linked-data/def/patent/Publication |