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Computer simulation of differential kinetics of MAPK activation upon EGF receptor overexpression

机译:EGF受体过表达对MAPK激活差分动力学的计算机模拟

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Everyday cells encounter various stimuli ranging from growth signals to bacterial infections to UV insult to death signals. They must somehow receive these signals, interpret them, integrate different stimuli, and generate the required output. They can do so by an intricate mechanism named intracellular signal transduction. There are various signal transduction pathways within a cell, each of which are designed for a particular stimulus, and all of which can crosstalk among themselves for the careful integration of all stimuli. In this report, only one of these pathways, the mitogen-activated protein kinase (MAPK) pathway has been simulated. This pathway is activated upon binding of growth factors to their respective cell surface-bound receptors. Activated receptors relay the incoming signal to the cell interior via a cascade of proteins, which are thought to be involved in both the amplification of the signal, and the specificity of the pathway. A generic MAPK pathway activated by the EGF (epidermal growth factor) and the effect of receptor overexpression has been studied, and consistent with experimental evidence, it is shown that the number of EGF receptors on the cell surface is a key factor in the response generated by the pathway.
机译:日常细胞遇到各种刺激,从生长信号到细菌感染到紫外线侮辱死亡信号。它们必须以某种方式接收这些信号,解释它们,集成不同的刺激,并生成所需的输出。它们可以通过名为细胞内信号转导的复杂机制来实现。电池内有各种信号转导途径,每个信号转导途径被设计用于特定刺激,并且所有这些都可以串扰串扰,以便仔细整合所有刺激。在本报告中,已经模拟了这些途径中的一种途径,丝裂原激活的蛋白激酶(MAPK)途径。在其各自的细胞表面结合受体结合到生长因子时,该途径被激活。活化受体通过级联的蛋白质将进入的信号转发到细胞内部,蛋白质被认为参与信号的放大以及途径的特异性。通过研究EGF(表皮生长因子)激活的通用MAPK途径和受体过表达的影响,并与实验证据一致,结果表明细胞表面上的EGF受体的数量是产生的响应中的关键因素通过途径。

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