| Project/Area Number |
07557165
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
医薬分子機能学
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| Research Institution | The University of Tokushima |
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Principal Investigator |
YAMAUTI Takasi Faculty of Pharm.sci., The University of Tokushima Professor, 薬学部, 教授 (90041813)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥19,200,000 (Direct Cost: ¥19,200,000)
Fiscal Year 1997: ¥5,900,000 (Direct Cost: ¥5,900,000)
Fiscal Year 1996: ¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 1995: ¥6,900,000 (Direct Cost: ¥6,900,000)
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| Keywords | Al_3 heimer's disese / Ca^<2+> / calmoclulin / tau protcin / phophorylition / protein kinase / clmed cell line / タウタンパク質 / アミロイドプレローサータンパク / アルツハイマー / タウ / 培養細胞 / 遺伝子導入 / 神経分化 |
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| Research Abstract |
Alzheimer's disease (AD) is the most common neurodegenerative disorder worldwide, causing progressive dementia and death in many millions of people. Neurofibrillary tangles are characteristic lesions found in the brain of AD.These tangles are composed of paired helical filaments (PHFs), and the major component is the microtubule-associated protein tau. PHF-tau is abnormally hyperphosphorylated in AD.In order to investigate the control of phosphorylation of tau protein, we studied in cultured cells and obtained some interesting results as follows ; (i) We constructed the expression vector of tau protein and protein kinases, and transfected them to neuroblastoma cells or embryonic carcinoma cells (cell line P-19). Cloned cells expressing tau protein or protein kinases were generated and isolated. (ii) Treatment of retinoic acid on P-19 cells increased the expression of CaM kinase II and induced to change the splicing pattern of the delta isoform of the kinase. (iii) Neurite outgrowth was stimulated in cells overexpressing CaM kinase II with protein kinase C inhibitors, indicating that differentiation and proliferation of neural cells were regulated by the activity of protein kinase C and CaM kinase II.
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