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KAKEN_26462318seika.pdf
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Title |
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ADAM10を介した骨・軟骨形成の制御機構
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ADAM10 オ カイシタ コツ・ナンコツ ケイセイ ノ セイギョ キコウ
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ADAM10 o kaishita kotsu nankotsu keisei no seigyo kiko
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Regulation of bone and cartilage formation by ADAM10
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依田, 昌樹
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ヨダ, マサキ
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Yoda, Masaki
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慶應義塾大学・医学部・助教
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Research team head
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科研費研究者番号 : 30464994
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堀内, 圭輔
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ホリウチ, ケイスケ
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Horiuchi, Keisuke
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慶應義塾大学・医学部・特任准教授
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Research team member
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科研費研究者番号 : 30327564
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2017
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科学研究費補助金研究成果報告書
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2016
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本研究では膜型メタロプロテアーゼADAM10による骨・軟骨形成および破骨細胞分化の制御機構を明らかにすることを目的とした。軟骨特異的にADAM10を欠損させたマウスの解析から, 軟骨細胞の最終分化にADAM10は必須であることが明らかとなった。また, 骨芽細胞特異的にADAM10を欠損させたマウスの解析から, ADAM10を骨芽細胞で欠損させると血液中のTSLP濃度が上昇し重篤な皮膚炎を発症することが明らかとなった。さらに, ADAM10を欠損させた破骨細胞前駆細胞を用いた分化誘導実験から, ADAM10の基質であるNotchレセプターからのシグナルが破骨細胞分化を完全に抑制することが明らかとなった。
In this study, we analyzed the regulation mechanisms of bone/cartilage formation and osteoclast differentiation by membrane type metalloprotease ADAM10. Analysis of mice abrogated ADAM10 in cartilage revealed that ADAM10 is essential for final differentiation of chondrocytes. In addition, analysis of osteoblast-specific ADAM10 deficient mice revealed that these mice indicated an increase in TSLP concentration in the serum and exhibited severe dermatitis. Furthermore, the experiment for osteoclast differentiation using osteoclast precursor lacking ADAM10 revealed that the signaling from Notch receptor, which is one of substrates for ADAM10, on the cell membrane of osteoclast precursor completely suppresses osteoclast differentiation.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2014~2016
課題番号 : 26462318
研究分野 : 骨・軟骨代謝
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