アディポネクチンの主要結合パートナーであるT-カデリンは,代謝組織におけるERKシグナル伝達を抑制する
Hirofumi Nagao1,2, Yuta Kondo2, Keitaro Kawada2
1Department of Metabolism and Atherosclerosis, Graduate School of Medicine, The University of Osaka, Suita, Osaka 565-0871, Japan.
まとめ
T-カデリンはERKシグナル伝達を抑制し,心臓および骨格筋のホメオスタシスに影響を与えます. アディポネクチンは,細胞内経路とエクソソーム生成に影響を与えるT-カデリンを維持する.
科学分野:
- 細胞生物学 細胞生物学
- 分子シグナル伝達です.
- メタボリック研究.
背景:
- T-カデリンはアディポネクチン結合パートナーであり,臓器保護効果があります.
- 代謝組織におけるT-カデリンによって誘発される細胞内シグナル伝達の変化は十分に理解されていません.
研究 の 目的:
- 細胞内信号伝達経路の調節におけるT-カデリンの役割を調査する.
- T-カデリンの心臓および骨格筋の恒常性に対する効果を明らかにする.
主な方法:
- T-カデリンのノックダウンと過剰発現による細胞培養実験 (C2C12ミオサイト,F2内皮細胞)
- ERK信号のダウンストリームターゲットを特定するためのプロテオミック分析.
- 心臓と骨格筋におけるT-カデリンのノックアウトを持つネズミのモデル.
主要な成果:
- T-カデリンは,培養細胞とネズミの組織におけるERK (細胞外信号調節キナーゼ) 信号伝達を抑制する.
- T-カデリンのノックダウンにより,ERKのリン酸化が増加し,下流目標のアップレギュレーションが行われました.
- ネズミのT-カデリン除去は,ERKシグナル伝達の増加,心筋縮,飢餓中に筋肉縮の変化をもたらしました.
結論:
- T-カデリンは細胞内信号伝達を調節し,特にERK経路を抑制します.
- T-カデリンは,心臓および骨格筋のホメオスタシスを維持する役割を果たします.
- アディポネクチンによって維持されるT-カデリンは,エクソソームの生成と細胞の信号伝達に影響を与えます.
キーワード:
ERKERK ERKERK ERKERK ERKERK ERKERK ERKERK ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKER ERKERGPI-アンカーとして,IGF-1受容体は,IGF-1の受容体として認識されています.T-カデリン (T-cadherin) とはアディポネクティニンとはさらに関連する動画
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