Fajmut Ales, Dobovisek Andrej, Brumen Milan
Faculty of Medicine, Department of Biophysics and Faculty of Education, Department of Physics, University of Maribor, Koroska cesta 160, SI-2000 Maribor, Slovenia.
J Chem Inf Model. 2005 Nov-Dec;45(6):1610-5. doi: 10.1021/ci050178a.
In this paper the 4-state latch bridge model proposed by Rembold and Murphy is expanded; first by incorporation of the analytical expression of Ca2+ dependent MLCK activation from the work of Kato et al. and second, by inclusion of the myosin dephosphorylation based on the Michaelis-Menten kinetics. The analysis of the proposed model and the comparison with the original model results as well as with the experimental data is presented. The model is able to predict the steady-state isometric stress and the myosin phosphorylation in dependence on steady cytosolic [Ca2+] as well as the temporal evolution of the system in dependence on the input Ca2+ signal in the form of biphasic transient, whereby our model results are in several aspects in better agreement with experimental observations.
在本文中，Rembold和Murphy提出的四态闩锁桥模型得到了扩展；首先纳入了Kato等人工作中Ca2+依赖性肌球蛋白轻链激酶（MLCK）激活的解析表达式，其次纳入了基于米氏动力学的肌球蛋白去磷酸化。本文给出了对所提出模型的分析以及与原始模型结果和实验数据的比较。该模型能够预测稳态等长张力以及依赖于稳定胞质[Ca2+]的肌球蛋白磷酸化，以及依赖于双相瞬态形式的输入Ca2+信号的系统时间演变，在此，我们的模型结果在几个方面与实验观察结果更吻合。
