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Caspases01:24

Caspases

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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...
12.4K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

6.3K
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...
6.3K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.4K
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...
6.4K
Apoptosis01:30

Apoptosis

11.2K
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...
11.2K
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

2.8K
The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
2.8K
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

3.7K
Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized...
3.7K

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相关实验视频

Updated: Jun 13, 2025

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction
08:41

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction

Published on: January 12, 2016

11.7K

活动依赖性突触消除需要caspase-3激活.

Zhou Yu1, Andrian Gutu1, Namsoo Kim1

  • 1Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, United States.

eLife
|June 10, 2025
PubMed
概括

酶-3的激活对于在大脑发育过程中去除多余的突触至关重要. 这一过程对于正常的神经电路的形成至关重要,并且可以提供对阿尔茨海默氏症等神经退行性疾病的保护.

科学领域:

  • 神经科学是一个神经科学.
  • 分子生物学分子生物学
  • 发展生物学 发展生物学

背景情况:

  • 在大脑发育过程中,突触最初会过度产生,然后通过活动依赖的过程被消除.
  • 将神经元活动与突触移除联系在一起的精确机制仍然不完全理解.
  • 较弱的突触优先被除,但分子参与者尚未完全阐明.

研究的目的:

  • 为了调查caspase-3在神经发育过程中的活动依赖突触消除中的作用.
  • 为了确定酶-3缺乏是否会影响由自发和经验依赖的神经活动驱动的突触消除.
  • 探索向caspase-3的潜力,以防止像阿尔茨海默病这样的神经退行性疾病中的突触损失.

主要方法:

  • 利用一个正在发展的小鼠视觉路径模型.
  • 操纵突触传输以诱导后突触caspase-3激活.
  • 产生了caspase-3缺乏的小鼠,以评估其在突触消除中的作用.
  • 检查了突触消除和不活跃突触的微质吞.
  • 在阿尔茨海默病的小鼠模型中研究了突触损失.

主要成果:

  • 抑制突触传输导致在发育中的小鼠视觉路径中的后突触caspase-3激活.
关键词:
卡斯帕斯-3酶是什么意思发育生物学是发展生物学.微质细胞中的微质细胞这里是鼠标鼠标鼠标鼠标鼠标鼠标.神经科学 神经科学突触的消除 突触的消除突触活动突触活动.

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  • 卡斯巴-3缺乏症会导致突触消除受自发和经验依赖的神经活动介导的损害.
  • 在caspase-3缺乏的小鼠中,活动依赖的突触消除被显著阻断,微质细胞对不活跃突触的吞减少.
  • 在阿尔茨海默病小鼠模型中,卡斯帕酶-3缺乏提供了对粉样蛋白β诱导的突触损失的保护.
  • 结论:

    • 酶-3激活是大脑发育期间活动依赖突触消除的关键分子事件.
    • 这些发现突出了caspase-3作为突触修剪的关键调节者.
    • 向caspase-3可能是缓解神经退行性疾病中突触损失的治疗策略.