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首页> 外文期刊>Biophysical Chemistry: An International Journal Devoted to the Physical Chemistry of Biological Phenomena >Mathematical analysis of binary activation of a cell cycle kinase which down-regulates its own inhibitor.
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Mathematical analysis of binary activation of a cell cycle kinase which down-regulates its own inhibitor.

机译：下调其自身抑制剂的细胞周期激酶的二元激活的数学分析。

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摘要

In mammalian cells, the heterodimeric kinase cyclin E/CDK2 (EK2) mediates cell cycle progress from G1 phase into S phase. The protein p27Kip1 (p27) binds to and inhibits EK2; but EK2 can phosphorylate p27, and that leads to the deactivation of p27, presumably liberating more EK2 and forming a positive-feedback loop. It has been proposed that this positive-feedback loop gives rise to binary (all-or-none) release of EK2 from its inactive complex with p27. Binary release suggests a bistable biochemical system in which a stable steady state with low EK2 activity is extinguished in a saddle-node bifurcation, causing the system to shift abruptly to a stable steady state with high EK2 activity. Two mathematical models are discussed, one in which free EK2 deactivates p27 in the EK2-p27 inhibitory complex as well as free p27, and one in which the rate of EK2-catalyzed deactivation of free p27 has saturable kinetics with respect to free p27. In general, if inhibitory binding is approximately in equilibrium, bistability requires that there be a potential unstable steady state where the reaction order of p27 deactivation is greater with respect to EK2 than with respect to p27.
机译：在哺乳动物细胞中，异二聚体激酶细胞周期蛋白E / CDK2（EK2）介导细胞周期从G1期进入S期。蛋白p27Kip1（p27）结合并抑制EK2;但是EK2可以使p27磷酸化，从而导致p27失活，大概释放出更多的EK2并形成正反馈回路。已经提出，该正反馈回路引起EK2从其与p27的非活性复合物中的二元（全或无）释放。二元释放表明是双稳态生化系统，其中具有低EK2活性的稳定稳态在鞍形节点分叉中熄灭，导致系统突然转变为具有高EK2活性的稳定稳态。讨论了两种数学模型，一种是游离EK2使EK2-p27抑制复合物中的p27失活，另一种是其中EK2催化的游离p27失活速率相对于游离p27具有饱和动力学。通常，如果抑制性结合大致处于平衡状态，则双稳态要求存在潜在的不稳定稳态，其中相对于EK2，p27失活的反应顺序要大于相对于p27。

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