Mahama P A, Linderman J J
Department of Chemical Engineering, University of Michigan, Ann Arbor 48109-2136.
Biophys J. 1994 Sep;67(3):1345-57. doi: 10.1016/S0006-3495(94)80606-X.
To link quantitatively the cell surface binding of ligand to receptor with the production of cellular responses, it may be necessary to explore early events in signal transduction such as G-protein activation. Two different model frameworks relating receptor/ligand binding to G-protein activation are examined. In the first framework, a simple ordinary differential equation model is used to describe receptor/ligand binding and G-protein activation. In the second framework, the events leading to G-protein activation are simulated using a dynamic Monte Carlo model. In both models, reactions between ligand-bound receptors and G-proteins are assumed to be diffusion-limited. The Monte Carlo model predicts two regimes of G-protein activation, depending upon whether the lifetime of a receptor/ligand complex is long or short compared with the time needed for diffusional encounters of complexes and G-proteins. When the lifetime of a complex is relatively short compared with the diffusion time, the movement of ligand among free receptors by binding and unbinding ("switching") significantly enhances G-protein activation. Receptor antagonists dramatically reduce G-protein activation and, thus, signal transduction in this case, and significant clustering of active G-proteins near receptor/ligand complexes results. The simple ordinary differential equation model poorly predicts G-protein activation for this situation. In the alternative case, when diffusion is relatively fast, ligand movement among receptors is less important and the simple ordinary differential equation model and Monte Carlo model results are similar. In this case, there is little clustering of active G-proteins near receptor/ligand complexes. Results also indicate that as the GTPase activity of the alpha-subunit decreases, the steady-state level of alpha-GTP increases, although temporal sensitivity is compromised.
为了定量地将配体与受体的细胞表面结合与细胞反应的产生联系起来,可能有必要探索信号转导的早期事件,如G蛋白激活。研究了两种将受体/配体结合与G蛋白激活相关联的不同模型框架。在第一个框架中,使用一个简单的常微分方程模型来描述受体/配体结合和G蛋白激活。在第二个框架中,使用动态蒙特卡罗模型模拟导致G蛋白激活的事件。在这两个模型中,假定配体结合的受体与G蛋白之间的反应是扩散受限的。蒙特卡罗模型预测了G蛋白激活的两种状态,这取决于受体/配体复合物的寿命与复合物和G蛋白扩散相遇所需时间相比是长还是短。当复合物的寿命与扩散时间相比相对较短时,配体通过结合和解离(“切换”)在游离受体之间的移动会显著增强G蛋白激活。在这种情况下,受体拮抗剂会显著降低G蛋白激活,从而降低信号转导,并且在受体/配体复合物附近会出现大量活性G蛋白聚集。对于这种情况,简单的常微分方程模型对G蛋白激活的预测效果很差。在另一种情况下,当扩散相对较快时,配体在受体之间的移动就不那么重要了,简单的常微分方程模型和蒙特卡罗模型的结果相似。在这种情况下,受体/配体复合物附近几乎没有活性G蛋白聚集。结果还表明,随着α亚基的GTP酶活性降低,α-GTP的稳态水平会升高,尽管时间敏感性会受到影响。