Project/Area Number |
08670310
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Bacteriology (including Mycology)
|
Research Institution | Sapporo Medical University |
Principal Investigator |
FUJII Nobuhiro Sapporo Medical University Microbiology Professor, 医学部, 教授 (90133719)
|
Co-Investigator(Kenkyū-buntansha) |
KIMURA Koichi Sapporo Medical University Microbiology Assisitant Prof., 医学部, 講師 (90177915)
YOKOSAWA Noriko Sapporo Medical University Microbiology Assistant Prof., 医学部, 講師 (50167722)
|
Project Period (FY) |
1996 – 1997
|
Project Status |
Completed (Fiscal Year 1997)
|
Budget Amount *help |
¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
|
Keywords | Botulinum toxin / SNAP-25 / Syntaxin / NG 108 / SK-N-F1 / ボツリヌスC型毒素 / ボツリヌスE型毒素 / 結合領域 / シンタキシン / SNAP25 / NT2 / 分化 |
Research Abstract |
Botulium type C neurotoxin was able to bind to NG 108 cells. Cellular sytaxin was clead in intact NG 108 cells treated with 0.5 to 50 nM of type C toxin for 48 to 96 hrs. ED 50 was 1.5 nM at the time of 96 hrs-treatment. The digestion and/or cleavage of syntaxin by the added-toxin was accelerated by chloroquine, but inhibited by cycloheximide or NH4Cl. Furthermore, several monoclonal antibodies, which inhibits the binding activity of toxin to NG 108 cells, prevented syntaxin from breake down caused by toxin. Type E neurotoxin was also able to bind to SK-N-F1 cells. Cellular SNAP-25 was cleaved by trypsin-treated neurotoxin.
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