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Master Transcription Regulators02:23

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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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mTORは,YY1-PGC-1alpha転写複合体を通してミトコンドリアの酸化機能を制御する.

John T Cunningham1, Joseph T Rodgers, Daniel H Arlow

  • 1Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.

Nature
|November 30, 2007
PubMed
まとめ

ラパミシン (mTOR) の哺乳類標的は,ミトコンドリアの酸化機能に不可欠である. mTORは,トランスクリプション因子YY1を通じてミトコンドリアの遺伝子発現と酸素消費を調節し,エネルギーホメオスタシスに影響を与えます.

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科学分野:

  • 細胞の代謝について
  • ミトコンドリア生物学
  • 分子内分泌学分子内分泌学

背景:

  • ペロキシソーム増殖器活性化受容体共同活性化剤 (PGC) -1αは,ミトコンドリアの酸化機能とエネルギーホメオスタシスを調節する.
  • ラパミシン (mTOR) の哺乳類標的は,栄養およびエネルギー経路における重要なキナーゼであり,細胞の成長と生存を制御します.
  • ミトコンドリアの酸化活動を調節するmTORの正確な役割は不明である.

研究 の 目的:

  • mTORがミトコンドリアの酸化活動を制御するかどうか,そしてどのように制御するかを調査する.
  • mTORシグナル伝達とミトコンドリアの機能を結びつける分子メカニズムを解明する.
  • 代謝疾患や癌の潜在的治療標的を特定する.

主な方法:

  • 骨格筋組織と細胞におけるラパミシンによるmTOR阻害を活用した.
  • ミトコンドリアの転写レギュレータ (PGC-1α,エストロゲン関連受容体α,核呼吸器系因子) の評価された遺伝子発現.
  • 転写因子標的を特定するために計算型ゲノミクスを採用し,その後,遺伝子ノックダウン研究とタンパク質-タンパク質相互作用アッセイを行った.

主要な成果:

  • mTOR抑制により,PGC-1α,エストロゲン関連受容体α,核呼吸因子の発現が低下し,ミトコンドリアの遺伝子発現と酸素消費が低下した.
  • yin-yang 1 (YY1) をmTORとPGC-1alpha.の共通の転写標的として特定した.
  • YY1のノックダウンにより,ミトコンドリアの遺伝子発現と呼吸が著しく低下し,YY1はmTOR阻害による遺伝子抑制に必要であった. mTORとラプターはYY1と相互作用し,mTORの阻害はYY1-PGC-1αの相互作用と同活性化を妨げました.

結論:

  • mTORは,ミトコンドリアの酸化機能を維持するために不可欠です.
  • 新しいメカニズムは,mTORシグナリングがYY1とPGC-1alpha.alphaの転写制御を通じてミトコンドリアの酸化機能を調節することを明らかにしています.
  • この経路は,エネルギー代謝のバランスをとるために不可欠であり,代謝疾患や癌に影響を及ぼします.