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相关概念视频

Caspases01:24

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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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The primary microtubule organizing center (MTOC) in animal cells is the centrosome. A centrosome has two cylindrical centrioles at its core. Each centriole consists of nine sets of three microtubules held together by proteins. The centrioles are positioned at right angles to each other and surrounded by a shapeless protein cloud called the pericentriolar matrix, or pericentriolar material (PCM).
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Most animal cells comprise a pair of centrioles together called a centrosome. The cell duplicates its centrosome and contains two centrosomes side-by-side, which begin to move apart during the prophase. As the centrosomes migrate to two different sides of the cell, microtubules start extending from each centrosome toward the other end. The mitotic spindle is composed of the centrosomes and their emerging microtubules.
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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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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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卡斯巴-2 杀死具有额外中心体的细胞.

Dario Rizzotto1, Vincenza Vigorito2, Patricia Rieder1

  • 1CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090 Vienna, Austria.

Science advances
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额外的中心体在细胞动力失败的血液细胞中触发了卡斯帕-2-驱动的亡,防止了致病性多倍化. 这种细胞死亡途径涉及PIDDosome复合体和BID处理,突出显示中心体.

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科学领域:

  • 细胞生物学 细胞生物学
  • 分子生物学分子生物学
  • 细胞亡研究研究

背景情况:

  • 中心体是关键的微管组织中心,对细胞功能至关重要.
  • 无法控制的中心细胞重复会导致基因组的不稳定性和疾病.
  • 细胞动力学失败可能导致多化,这种状态与病变发生有关.

研究的目的:

  • 为了研究细胞运动失败后细胞死亡中中心体的作用.
  • 阐明将额外的中心体与亡联系起来的分子机制.
  • 了解细胞是如何防止致病性多化.

主要方法:

  • 对经历了细胞动力学失败的血细胞进行分析.
  • 研究caspase-2激活及其对PIDDosome复合体的依赖.
  • 利用基因操纵 (例如,ANKRD26,BID缺陷) 来研究细胞存活率和细胞亡.
  • 检查线粒体外膜通透性 (MOMP) 和p53依赖的通路.

主要成果:

  • 额外的中心体是必要的,以触发失败的细胞中卡斯巴-2-驱动的亡.
  • 在额外的中心细胞中,PIDD1的原始化对于卡斯巴酶-2通路的激活至关重要.
  • 丢失ANKRD26允许细胞存活和多化.
  • 卡斯巴-2处理BID,启动BAX/BAK依赖的MOMP.
  • 缺乏BID的细胞通过caspase-2激活了p53依赖的亡.

结论:

  • 中心体通过诱导PIDDosome驱动的亡来限制它们自己的非计划复制.
  • 这种机制可以防止潜在的致病性多聚化事件.
  • 这项研究揭示了中枢细胞在调节细胞命运和预防体积的过程中扮演的新角色.