Autoimmune neurological diseases targeting neuronal acetylcholine receptor
Project/Area Number |
24591253
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurology
|
Research Institution | Kanazawa University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
YOKOYAMA Shigeru 金沢大学, 子どものこころの発達研究センター, 教授 (00210633)
|
Co-Investigator(Renkei-kenkyūsha) |
ADACHI Yumi 金沢大学, 保健管理センター, 准教授 (30447677)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 自己免疫疾患 / 自律神経機能障害 / アセチルコリン受容体 / 細胞内カルシウム濃度 / エンドサイトーシス / 重症筋無力症 / 自律神経 / 自己抗体 / 神経型アセチルコリン受容体 / 免疫性神経疾患 / 自己免疫 / 神経細胞 |
Outline of Final Research Achievements |
There are patients with autoantibodies for neuronal acetylcholine receptor (nAChR alpha 3 subunit) with autonomic nervous system dysfunction. We used excessive expression cells of nAChR (alpha-3 and beta-4), and investigated the effects of patient’s serum and monoclonal anti-alpha-3 antibodies. Patient serum containing medium induced internalization of nAChR (alpha-3 and beta-4) into the cytoplasm. Monoclonal anti-alpha-3 antibodies decreased the expression of alpha-3 subunit and reduced the concentration of Ca2+ in cytoplasm. Processing at 4 °C revealed no decrease of alpha-3 subunit on the surface, that indicated endocytosis had a role in the process of decrease of alpha-3 subunits on the cell surface.
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Report
(4 results)
Research Products
(36 results)