| Project/Area Number |
08457610
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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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) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 1997: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1996: ¥4,200,000 (Direct Cost: ¥4,200,000)
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| Keywords | Ca^<2+> / calmodulis / protein kinase / protein phosphorylatiom / neuroklastoma / gene transfection / signal transduction / カルチデュリン |
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| Research Abstract |
Neuronal CaM kinase II plays some important roles in the control of nerve functions in response to intracellular Ca^<2+>. In this study, we compared the effect of overexpression of the beta isoform of CaM kinase II with that of the alpha isoform, since the alpha and beta isoforms of CaM kinase II are known to be expressed almost exclusively in the brain. We obtained the following results ; (i) the subcellulr distribution of the alpha isoform was different from that of the beta isoform, although the catalytic properties of the alpha and beta isoforms expressed in transfected cells were similar to those of brain CaM kinase II ; (ii) the alpha isoform was found in the soluble fraction more than in the particulate fraction, whereas most the beta isoform bound to subcellular structures ; (iii) in the cell overexpressing alpha and beta isoforms of CaM kinase II,neurite extension was promoted when compared with the morphology of neo transfectants ; (iv) neurite outgrowth of cells overexpressing CaM kinase II was further stimulated by the inhibitor of protein kinase C ; (v) morphological changes were greater in the beta cells than in the alpha cells ; (vi) some substrates of CaM kinase II related to neurite outgrowth, were detected in cells overexpressing CaM kinase II stimulated with H-7.
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