| Project/Area Number |
17590902
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | FUJITA HEALTH UNIVERSITY |
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Principal Investigator |
MUTOH Tatsuro FUJITA HEALTH UNIVERSITY, School of Medicine, Professor, 医学部, 教授 (60190857)
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| Co-Investigator(Kenkyū-buntansha) |
KUSUNOKI Susumu KINNKI UNIVERSITY, School of Medicine, Professor, 医学部, 教授 (90195438)
YAMAMOTO Hiroko FUJITA HEALTH UNIVERSITY, School of Medicine, Professor, 医学部, 教授 (20148258)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2005: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | signal transduction / GBS / nerve growth factor / Trk / tyrosine kinase / tyrosine phosphorylation / glucosylceramide / PC12 cells / GM1 / チロシン自己燐酸化 / 中性糖脂質 / MAPK |
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| Research Abstract |
Previous studies have shown that anti-ganglioside antibody such as anti-GM1 antibody has been postulated to have the pathognomonic implication for the development of clinical GBS-like phenotype. At present, however, the detailed molecular mechanisms and significances of these anti-ganglioside antibodies. In this project, we examined the molecular effects of these antibodies on the function of high affinity nerve growth factor (NGF) receptor, Trk and disclosed as follows ; 1)anti-GM1 antibodies differently affected the function of Trk activity among these antibodies, some augmented NGF-induced Trk autophosphorylation, the other inhibited it. 2)In whole cell culture system, these antibody-positive sera differently stimulated the intracellular signaling molecules that are involved in the intracellular signal transduction cascade. These data suggested that anti-GM1 antibody from different patients is not always identical and it affected the function of Trk-mediated intracellular signaling machinery.
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