ヒストン脱酸化酵素Sirt6は,Hif1alpha経由でグルコースホメオスタシスを調節する
Lei Zhong1, Agustina D'Urso, Debra Toiber
1The Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA.
Cell
|February 10, 2010
まとめ
この研究では,SIRT6タンパク質は,グリコリチス遺伝子を調節することによって,グルコースレベルを制御することを明らかにしました. SIRT6欠乏症は低血糖症を引き起こし,グルコースホメオスタシスと代謝疾患の治療に影響を及ぼします.
科学分野:
- バイオケミストリー バイオケミストリー
- 分子生物学は分子生物学である.
- 遺伝学 遺伝学とは
背景:
- SIRT6は,代謝とストレス耐性に関与するNAD (((+)) 依存型脱酸化酵素である.
- SIRT6欠乏したマウスは致死性低血糖症を発症しますが,その根本的なメカニズムは不明です.
研究 の 目的:
- グルコースホメオスタシスにおけるSIRT6の役割を明らかにする.
- SIRT6欠乏が低血糖を引き起こすメカニズムを調査する.
主な方法:
- ヒストンデセチラゼ検査. ヒストンデセチラゼ検査.
- 遺伝子発現分析. 遺伝子発現分析. 遺伝子発現分析. 遺伝子発現分析.
- SIRT6欠乏細胞とマウスにおける細胞のグルコース吸収と代謝の分析.
主要な成果:
- SIRT6はヒストンH3K9脱酸化酵素として作用し,糖質性遺伝子発現を調節する.
- SIRT6は,低酸素誘導因子1-α (Hif1alpha) のコアプレッサーとして機能する.
- SIRT6欠乏症は,Hif1alphaの活性が増加し,糖分解が強化され,グルコースの吸収が増加し,ミトコンドリアの呼吸が低下する.
結論:
- SIRT6は,糖質性遺伝子発現の制御を通じて,グルコースホメオスタシスの主要な調節体です.
- SIRT6がHif1alphaと糖分解を調節する役割は,糖尿病や肥満などの代謝疾患に対する潜在的な治療標的を提供します.
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