Niv Masha Y, Skrabanek Lucy, Filizola Marta, Weinstein Harel
Department of Physiology and Biophysics, Weill Medical College of Cornell University, 1300 York Ave., New York, NY 10021, USA.
J Comput Aided Mol Des. 2006 Jul-Aug;20(7-8):437-48. doi: 10.1007/s10822-006-9061-3. Epub 2006 Nov 11.
Activation of G Protein-Coupled Receptors (GPCRs) is an allosteric mechanism triggered by ligand binding and resulting in conformational changes transduced by the transmembrane domain. Models of the activated forms of GPCRs have become increasingly necessary for the development of a clear understanding of signal propagation into the cell. Experimental evidence points to a multiplicity of conformations related to the activation of the receptor, rendered important physiologically by the suggestion that different conformations may be responsible for coupling to different signaling pathways. In contrast to the inactive state of rhodopsin (RHO) for which several high quality X-ray structures are available, the structure-related information for the active states of rhodopsin and all other GPCRs is indirect. We have collected and stored such information in a repository we maintain for activation-specific structural data available for rhodopsin-like GPCRs, http://www.physiology.med.cornell.edu/GPCRactivation/gpcrindex.html . Using these data as structural constraints, we have applied Simulated Annealing Molecular Dynamics to construct a number of different active state models of RHO starting from the known inactive structure. The common features of the models indicate that TM3 and TM5 play an important role in activation, in addition to the well-established rearrangement of TM6. Some of the structural changes observed in these models occur in regions that were not involved in the constraints, and have not been previously tested experimentally; they emerge as interesting candidates for further experimental exploration of the conformational space of activated GPCRs. We show that none of the normal modes calculated from the inactive structure has a dominant contribution along the path of conformational rearrangement from inactive to the active forms of RHO in the models. This result may differentiate rhodopsin from other GPCRs, and the reasons for this difference are discussed in the context of the structural properties and the physiological function of the protein.
G蛋白偶联受体(GPCRs)的激活是一种由配体结合触发的变构机制,导致跨膜结构域传导构象变化。对于清晰理解信号向细胞内的传播而言,GPCRs激活形式的模型变得愈发必要。实验证据表明,与受体激活相关的构象具有多样性,鉴于不同构象可能负责与不同信号通路偶联这一观点,这些构象在生理上具有重要意义。与已有多个高质量X射线结构的视紫红质(RHO)非活性状态不同,视紫红质和所有其他GPCRs活性状态的结构相关信息是间接的。我们已将此类信息收集并存储在一个我们维护的储存库中,该储存库提供视紫红质样GPCRs激活特异性结构数据,网址为http://www.physiology.med.cornell.edu/GPCRactivation/gpcrindex.html 。利用这些数据作为结构限制条件,我们应用模拟退火分子动力学从已知的非活性结构出发构建了多个不同的RHO活性状态模型。这些模型的共同特征表明,除了TM6既定的重排外,TM3和TM5在激活过程中也发挥着重要作用。在这些模型中观察到的一些结构变化发生在未涉及限制条件且此前未进行过实验测试的区域;它们成为进一步实验探索激活型GPCRs构象空间的有趣候选对象。我们表明,从非活性结构计算出的正常模式在模型中从RHO的非活性形式到活性形式的构象重排路径上均无主导贡献。这一结果可能使视紫红质与其他GPCRs有所区别,本文将在蛋白质的结构特性和生理功能背景下讨论这种差异的原因。