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相关概念视频

The Intrinsic Apoptotic Pathway01:31

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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...
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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...
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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...
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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...
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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. 
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有关炎症的亡 (proinflammatory apoptosis) 是一种促炎症的亡.

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概括
此摘要是机器生成的。

在上皮质中剩余的亡细胞触发炎症. 这些细胞释放腺三酸盐 (ATP),这是一个危险信号,激活炎症反应.

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科学领域:

  • 细胞生物学 细胞生物学
  • 免疫学 免疫学 免疫学
  • 皮质生物学 皮质生物学

背景情况:

  • 细胞亡是被编程的细胞死亡,对于组织平衡至关重要.
  • 失败的细胞清除可以导致炎症状况.
  • 表皮细胞形成屏障,并不断更新.

研究的目的:

  • 为了研究未被清除的细胞在上皮质炎症中的作用.
  • 为了确定由此apoptotic细胞诱导炎症的分子机制.

主要方法:

  • 使用了体外上皮质模型.
  • 采用技术来诱导和防止细胞亡的细胞清除.
  • 测量了炎症媒介释放和信号通路.

主要成果:

  • 在上皮内保留的亡细胞释放出大量的三氨酸腺酸盐 (ATP).
  • 这些细胞中的细胞外ATP激活了邻近的上皮细胞和免疫细胞上的纯能受体.
  • 这种激活启动了促炎信号级联.

结论:

  • 表皮中的未被清除的亡细胞是炎症信号的来源.
  • 这些细胞释放的ATP是驱动炎症的关键机制.
  • 准ATP信号传递可能为上皮质炎症提供治疗策略.