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Analysis of Cell Cycle Position in Mammalian Cells
Published on: January 21, 2012
RBタンパク質によって誘発されるG1相停止のc-mycによる無効化がp53によって誘発されるが,p53によって誘発されない
1Center for Molecular Medicine, University of Texas Health Science Center, San Antonio 78245.
Nature
|November 12, 1992
まとめ
レチノブラストーマ (RB) タンパク質は,通常,細胞の成長を止めます. しかし,c-mycタンパク質は,このRB機能を無視し,細胞増殖を促進します. この研究は,細胞調節におけるc-mycとRBの間の特定の対抗性を明らかにしています.
科学分野:
- 分子生物学は分子生物学である.
- がん研究 がん研究
- 細胞サイクル規則 細胞サイクル規則
背景:
- 網膜芽細胞腫遺伝子 (RB) の不活性化変異は,様々な腫瘍に共通しています.
- RBタンパク質 (Rb) は,細胞の成長を否定的に調節することによって,腫瘍抑制剤として作用します.
- c-myc腫瘍遺伝子の活性化により,細胞増殖が促進され,分化が阻害され,成長の正の調節作用が示唆される.
研究 の 目的:
- RBタンパク質とc-myc.c.c.の機能的相互作用を調査する.
- c-mycが,RB.の細胞サイクル停止機能に敵対するかどうかを判断する.
- 他のオンコタンパク質と対照的に,c-mycとRBの相互作用の特異性を調査する.
主な方法:
- 精製されたRBタンパク質を細胞に微量注入する.
- RBタンパク質とC-myc,EJ-ras,C-fos,C-junなど様々なオンコプロテインを同時に注入する.
- マイクロインジェクション後の細胞サイクル進行の評価.
主要な成果:
- 単独のRBタンパク質のマイクロ注射は,G1フェーズにおける可逆的な細胞サイクル停止を引き起こした.
- c-mycとRBの併用注射は,RBの細胞サイクルを停止する能力を阻害しました.
- EJ-ras,c-fos,またはc-junの併用は,RBの細胞サイクル停止機能に影響を与えませんでした.
- c-mycはp53.3の腫瘍抑制活性を抑制しませんでした.
結論:
- c-mycは,RB.の腫瘍抑制機能に特異的に敵対する.
- c-mycとRBの間のこの機能的対抗性は,細胞増殖と潜在的に腫瘍発生に役割を果たします.
- この相互作用は,細胞サイクル制御と癌の発症における重要な分子メカニズムを強調しています.
関連する概念動画
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Abnormal Proliferation
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The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
DNA Damage Can Stall the Cell Cycle
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

