新型ATM関連タンパク質TRRAPは,c-MycおよびE2Fオンコプロテインの重要なコファクターである
S B McMahon1, H A Van Buskirk, K A Dugan
1Department of Molecular Biology, Princeton University, New Jersey 08544-1014, USA.
Cell
|August 26, 1998
まとめ
研究者は,c-MycとE2F-1と相互作用するタンパク質であるTRRAPを特定しました. TRRAP機能をブロックすると,腫瘍性変異が抑制され,これらの経路におけるコファクターとしての重要な役割が示唆されます.
科学分野:
- 分子生物学は分子生物学である.
- 細胞サイクル規制について
- 腫瘍生成 (オンコゲネシス) について
背景:
- c-MycとE2Fの転写因子は,細胞サイクル進行の重要な調節因子である.
- 彼らの経路に関与するコファクターを理解することは,腫瘍性変異の理解に不可欠です.
研究 の 目的:
- c-MycとE2F-1と相互作用する新しいタンパク質を分離し,特徴づけること.
- これらの相互作用するタンパク質が腫瘍性変異における役割を調査する.
主な方法:
- タンパク質の分離と特徴づけ.
- 同免疫プレシピテーションアッセイは,タンパク質の相互作用を研究するためのものです.
- トランスドミナント変異体とアンチセンセスのRNAを用いた機能研究.
主要な成果:
- 新しい,保存された434 kDaのタンパク質,TRRAPが特定されました.
- TRRAPは,特にc-MycのN端末とE2F-1トランザクティベーションドメインと相互作用する.
- TRRAPはATM/PI3-キナーゼファミリーと同質性を示しています.
- TRRAP機能の抑制により,c-MycおよびE1A媒介による腫瘍性変異が阻害されました.
結論:
- TRRAPは,c-MycとE1A/E2Fの両方の転写因子経路のための新しい,重要なコファクターです.
- TRRAPは,細胞サイクル進行を調節し,腫瘍性変異を防止する上で重要な役割を果たします.
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