関連する実験動画
Updated: Jun 6, 2026

08:35
Examining BCL-2 Family Function with Large Unilamellar Vesicles
Published on: October 5, 2012
BID,BIM,およびPUMAは,BAXおよびBAKに依存する細胞死プログラムの活性化に不可欠です
Decheng Ren1, Ho-Chou Tu, Hyungjin Kim
1Molecular Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
まとめ
タンパク質BID,BIM,PUMAは,アポトーシスを開始する重要なタンパク質であるBAXとBAKを活性化するために不可欠です. ノックアウトマウスにおけるそれらの欠乏は,バックスとバックの欠乏を反映し,細胞死信号を防ぐ.
科学分野:
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
- 遺伝学 遺伝学とは
背景:
- ミトコンドリアのアポトーシスの開始は,BAXとBAKタンパク質に依存しています.
- BAXとBAKの正確な活性化メカニズムは不明である.
研究 の 目的:
- BAXとBAKの活性化におけるBID,BIM,PUMAのインビボの役割を調査する.
- アポトーシスにおけるBAXとBAKのアップストリームアクティベータを解明する.
主な方法:
- Bid,Bim,Pumaを欠いたトリプルノックアウトマウスを使った.
- ノックアウトモデルにおける発達障害とアポトーシスシグナル伝達経路の分析.
- BAXとBAKのホモオリゴメリゼーションとカスパース活性化の評価.
主要な成果:
- Bid,Bim,Pumaのトリプルノックアウトマウスは,バックスとバックの欠陥に似た発達障害を示した.
- BID,BIM,PUMAの遺伝子削除は,BAXとBAKのホモオリゴメリゼーションを阻害しました.
- これらのノックアウト細胞では,他のBH3のみのタンパク質が存在しているにもかかわらず,シトクロームc媒介のカスパース活性化が防止されました.
結論:
- BID,BIM,PUMAはミトコンドリアでBAXとBAKを直接活性化する.
- これらのタンパク質は,様々な死の信号に反応してアポトーシスを開始するために不可欠です.
- 多くの形態のアポトーシスは,BID,BIM,またはPUMAファミリータンパク質によるBAXとBAKの直接的なミトコンドリア活性化に依存しています.
関連する概念動画
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...
Cellular Injury V: Apoptosis and Autophagy
Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
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...
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.
Autophagic Cell Death
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
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.

