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Mathematical Model Explaining the Role of CDC6 in the Diauxic Growth of CDK1 Activity during the M-Phase of the Cell Cycle

机译:数学模型解释CDC6在细胞周期M期中CDK1活性的双生生长中的作用

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摘要

In this paper we propose a role for the protein in the entry of cells into mitosis. This has not been considered in the literature so far. Recent experiments suggest that , upon entry into mitosis, inhibits the appearance of active and cyclin B complexes. This paper proposes a mathematical model which incorporates the dynamics of kinase , its regulatory protein cyclin B, the regulatory phosphatase and the inhibitor known to be involved in the regulation of active and cyclin B complexes. The experimental data lead us to formulate a new hypothesis that slows down the activation of inactive complexes of and cyclin B upon mitotic entry. Our mathematical model, based on mass action kinetics, provides a possible explanation for the experimental data. We claim that the dynamics of active complexes and cyclin B have a similar nature to diauxic dynamics introduced by Monod in 1949. In mathematical terms we state it as the existence of more than one inflection point of the curve defining the dynamics of the complexes.
机译:在本文中,我们提出了蛋白质在细胞进入有丝分裂中的作用。到目前为止,文献中尚未考虑到这一点。最近的实验表明,进入有丝分裂后,抑制了活性和细胞周期蛋白B复合物的出现。本文提出了一个数学模型,其中包含了激酶,其调节蛋白cyclin B,调节磷酸酶和已知参与活性和cyclin B复合物调节的抑制剂的动力学。实验数据使我们提出了一个新的假设,该假设减缓了有丝分裂进入后细胞周期蛋白和细胞周期蛋白B的非活性复合物的激活。我们基于质量动力学的数学模型为实验数据提供了可能的解释。我们声称活性复合物和细胞周期蛋白B的动力学性质与1949年Monod引入的双分子动力学性质相似。用数学术语来说,我们将其描述为定义复合物动力学的曲线存在多个拐点。

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