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疟疾与细胞周期

Malaria and the cell cycle.

作者信息

Leete T H, Rubin H

机构信息

Department of Medicine, Infectious Diseases Section, University of Pennsylvania, Philadelphia, PA 19104-6073, USA.

出版信息

Parasitol Today. 1996 Nov;12(11):442-4. doi: 10.1016/0169-4758(96)10068-5.

Abstract

The current model of cell cycle control features a succession of active cyclin-CDK (cyclin-dependent kinase) complexes, where accumulation of each successive cyclin leads to activation of its associated kinase. Cell fusion experiments have shown that nuclei sharing common cytoplasm progress through the cell cycle in synchrony. During schizogony of Plasmodium falciparum, nuclear division occurs asynchronously, and thus cannot be regulated by synthesis and accumulation of cyclins in the cytoplasm. We suggest that schizonts must have a ready pool of cyclins for activating all stages of the cycle, and that the cell cycle is regulated independently in each nucleus.

摘要

当前的细胞周期调控模型以一系列活性细胞周期蛋白 - 细胞周期蛋白依赖性激酶(CDK)复合物为特征,其中每个相继的细胞周期蛋白的积累会导致其相关激酶的激活。细胞融合实验表明,共享共同细胞质的细胞核会同步进行细胞周期。在恶性疟原虫的裂体生殖过程中,核分裂是异步发生的,因此无法通过细胞质中细胞周期蛋白的合成和积累来调控。我们认为,裂殖体必须有一个现成的细胞周期蛋白库来激活周期的所有阶段,并且细胞周期在每个细胞核中是独立调控的。

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