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相关概念视频

Inhibition of Cdk Activity02:34

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
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The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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CDK基质化和细胞循环的排序

Matthew P Swaffer1, Andrew W Jones2, Helen R Flynn3

  • 1Cell Cycle Laboratory, The Francis Crick Institute, London NW1 1AT, UK.

Cell
|December 17, 2016
PubMed
概括
此摘要是机器生成的。

单个循环依赖激酶 (CDK) 复合体可以通过精确控制基质化来暂时安排细胞循环事件. 增加的CDK活性和基质敏感性产生了不同的值,确保了细胞分裂的正常进展.

关键词:
美国S 阶段细胞周期环林依赖性激酶基因酶细胞分裂蛋白质组学化

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科学领域:

  • 细胞生物学
  • 分子生物学
  • 生物化学

背景情况:

  • 细胞循环的进展依赖于循环素依赖性激酶 (CDK) 综合体.
  • 在细胞分裂过程中,S阶段和细胞分裂的时间顺序至关重要.
  • 之前的模型表明CDK总活性水平,而不是基质特异性,决定细胞周期时间.

研究的目的:

  • 研究CDK基质在细胞周期中的时间排序.
  • 确定CDK活动水平和基质敏感度在细胞循环调节中的作用.
  • 在裂变酵母中分析CDK基质酸化模式.

主要方法:

  • 在裂变酵母中对CDK基质的基于蛋白学的系统分析.
  • 与野生细胞进行比较分析.
  • 测量CDK活性和基质化动态.

主要成果:

  • 一个单个环素-CDK复合物可以暂时命令不同基质的酸化.
  • 增加的CDK活性和差异化的基质灵敏度会产生特定的活性值.
  • 快速的化循环确保了细胞周期事件的特异性基质活性值.

结论:

  • 细胞周期事件的时间排序的关键机制是CDK活性水平和基质敏感性.
  • 循环基质特异性和活性值共同调整化模式.
  • 这种机制确保了下游细胞周期事件的精确执行.