CLOCK媒介によるBMAL1のアセチル化により,昼間の機能が制御されます.
Jun Hirayama1, Saurabh Sahar, Benedetto Grimaldi
1Department of Pharmacology, School of Medicine, University of California Irvine, Irvine 92697-4625, California, USA.
Nature
|December 14, 2007
まとめ
CLOCKタンパク質は,そのパートナーであるBMAL1をアセチル化し,これは体内時計の調節における重要なステップです. このアセチル化は,昼夜リズムと遺伝子発現の適切な機能に不可欠です.
科学分野:
- 分子生物学は分子生物学である.
- クロノバイオロジーはクロノバイオロジーを用います.
- エピジェネティクス エピジェネティクス
背景:
- シルカディアンリズムは,トランスクリプション・トランスレーション・フィードバック・ループによって調節されます.
- CLOCK-BMAL1複合体は遺伝子発現を活性化し,暗号染色体 (Crys) はそれを抑制する.
- CLOCKにはヒトロンアセチルトランスフェラーゼの内在的な活性があり,遺伝子発現に影響を与えます.
研究 の 目的:
- CLOCK.の非ヒストロンアセチル化作用を調査する.
- 昼夜リズム調節におけるBMAL1アセチル化の役割を決定する.
主な方法:
- マウスの肝臓におけるBMAL1アセチル化の分析.
- BMAL1.1における保存されたライシン537残基の変異.
- 細胞モデルのサーカディアンリズムを評価する. 救出.
主要な成果:
- CLOCKはライシン537でBMAL1を直接アセチル化する.
- BMAL1のアセチル化はリズム的であり,マウスの肝臓で発生する.
- アセチル化されたBMAL1はCRY1のリクルートを強化し,転写抑制を促進します.
- K537Rに変異したBMAL1は,昼夜リズムを回復できない.
結論:
- CLOCK-BMAL1の酵素相互作用は,昼夜機能に不可欠である.
- CLOCKによるBMAL1アセチル化が重要な規制メカニズムである.
- この翻訳後の改変は,昼間の遺伝子発現を微調整する.
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