関連する実験動画
Updated: Jun 18, 2026

07:42
Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Smacはミトコンドリアのタンパク質で,IAP阻害を排除することによって,シトクロームc依存カスパース活性化を促進する
1Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, 75235, USA.
Cell
|August 10, 2000
まとめ
新種のミトコンドリアタンパク質であるSmac (Second Mitochondria-derived Activator of Caspases) は,カスパスを活性化することでアポトシスを促進する. Smacは阻害タンパク質を中和し,プログラムされた細胞死シグナル伝達経路を強化します.
科学分野:
- バイオケミストリー バイオケミストリー
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
背景:
- アポトーシス,またはプログラム細胞死は,重要な細胞プロセスです.
- カスパゼの活性化は,アポプトシスの実行の中心的なものです.
- アポトーシスタンパク質の阻害剤 (IAP) はカスパースの活性を調節し,細胞死を予防します.
研究 の 目的:
- アポトーシス中のカスパース活性化に関与する新しいタンパク質を特定する.
- Smacがアポプトシス経路に影響を与えるメカニズムを解明する.
主な方法:
- タンパク質の識別と特徴付け.
- タンパク質とタンパク質の相互作用の分析.
- 細胞の局所化に関する研究.
- カスパース活性化とアポトーシスに対するSmacの効果の評価.
主要な成果:
- 新型ミトコンドリアタンパク質であるSmacの識別.
- Smacは,IAPsを敵対することによって,カスパーゼ-9の活性化を促進する.
- ミトコンドリアの局所化とシグナルペプチド分裂は,Smacのプロアポプトティック機能に不可欠です.
- Smacの過剰発現は,細胞をアポプトティック刺激に敏感にする.
結論:
- Smacはアポトーシスの重要な媒介体であり,ミトコンドリア外膜の浸透性の下流に作用する.
- Smacは,カスパースの活性化を促進するために,シトクロームcに類似して機能します.
- Smacは,アポトーシスを調節するための新しい標的を表しています.
関連する概念動画
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Apoptosis
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Caspases
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
The Extrinsic Apoptotic Pathway
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
The Intrinsic Apoptotic Pathway
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

