一种用于模拟细胞周期蛋白依赖性激酶（CDK）介导的磷酸化作用以及ARF（急性早幼粒细胞白血病相关因子）介导的p53转录活性稳定作用的联合途径。

A combined pathway to simulate CDK-dependent phosphorylation and ARF-dependent stabilization for p53 transcriptional activity.

作者信息

Doi Atsushi, Nagasaki Masao, Ueno Kazuko, Matsuno Hiroshi, Miyano Satoru

机构信息

Human Genome Center, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.

出版信息

Genome Inform. 2006;17(1):112-23.

PMID:17503361

Abstract

The protein p53 is phosphorylated by a member of protein kinases such as CDK7, and stabilized by the protein ARF. The phosphorylation and stabilization of p53 is believed to enhance its transcriptional activity and act simultaneously. Biological pathways composed of experts knowledge obtained from the literature are including these activation mechanisms. However, the map of biological pathways does not reflect the combination effect of phosphorylation and stabilization. We have conducted some simulations of biological pathways with hybrid functional Petri net (HFPN) after careful reading of papers. In this paper, we constructed the HFPN based biological pathway of CDK-dependent phosphorylation pathway and combine with ARF-dependent pathway described previously, to observe the effect of the phosphorylation on the stabilization with simulation-based validation.

摘要

蛋白质p53可被诸如CDK7等蛋白激酶成员磷酸化，并由蛋白ARF使其稳定。p53的磷酸化和稳定被认为可增强其转录活性且同时发挥作用。由从文献中获取的专家知识组成的生物途径包括这些激活机制。然而，生物途径图并未反映磷酸化和稳定的联合效应。在仔细阅读论文后，我们用混合功能Petri网（HFPN）对生物途径进行了一些模拟。在本文中，我们构建了基于HFPN的CDK依赖性磷酸化途径的生物途径，并与先前描述的ARF依赖性途径相结合，以通过基于模拟的验证来观察磷酸化对稳定的影响。