| Project/Area Number |
16590142
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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 |
General anatomy (including Histology/Embryology)
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| Research Institution | Mie University |
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Principal Investigator |
MIZOGUCHI Akira Mie University, Department of Anatomy, School of Medicine, Professor, 大学院・医学系研究科, 教授 (90181916)
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| Co-Investigator(Kenkyū-buntansha) |
KIMURA Kazushi Mie University, Department of Anatomy, School of Medicine, Assistant Professor, 大学院・医学系研究科, 講師 (20314180)
栢原 哲郎 三重大学, 医学部, 講師 (20024705)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Cell adhesion / Synapse formation / Nectin / Immuno globulin / Margarita Island syndrome / Mental retardation / Memory formation / Hippocampus / 精神発達遅延 / シナプス / マイクロアレイ |
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| Research Abstract |
Nectins are Ca^<2+>-independent immunoglobulin-like cell-cell adhesion molecules and comprise a family of four members. At the mossy fiber terminals of hippocampus, nectin-1 and nectin-3 localize at the presynaptic and postsynaptic sides of synaptic junctions, respectively, and their trans-interaction plays a role in formation of synapses in cooperation with N-cadherin. Nectins are associated with the actin cytoskeleton through afadin, a nectin- and actin filament-binding protein. Inhibition of nectin-1-and nectin-3-based adhesion by in nectin-1 -/- mice resulted in the abnormal formation of synapses (Honda et al., 2006). Taken together, it is likely that nectins are involved in the formation of synapses in cooperation with N-cadherin. This role of nectins is consistent with the finding that mutations in the nectin-1 gene are responsible for cleft lip/palate-ectodermal dysplasia, which is characterized by mental retardation in addition to ectodermal dysplasia.
For identification of a novel molecule that have cell-aggregation activity and is involved in synapse formation, we made a subtraction library for developmental hippocampus (P10-P5). This library was transfected into fibroblasts and the transfected cells were performed with cell-aggregation assay. We identified a voltage-gated K^+ channel as a cell adhesion molecule (Kimura et al., in preparation for submission). Furthermore, we also found that aquaproin 4, a water channel, has cell aggregation activity (Hiroaki et al. 2006).
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