Impact of salt bridges on the equilibrium binding and adhesion of human CD2 and CD58

Impact of salt bridges on the equilibrium binding and adhesion of human CD2 and CD58
复制标题

DOI:
10.1074/jbc.m607968200
复制
发表时间:
2007-02-23
影响因子:
4.8
通讯作者:
Leckband, Deborah E.
Leckband, Deborah E.
中科院分区:
生物学2区
文献类型:
--
作者:
Bayas, Marco V.;Kearney, Alice;Leckband, Deborah E.

文献摘要

被引文献

相似文献

本研究描述了单电荷突变对CD2-CD58相互作用的平衡结合、动力学和粘附强度的影响的定量研究。先前的分子动力学模拟指导了所研究的电荷突变体的选择,包括CD2突变体D31A, K41A, K51A和K91A。这一组包括突变,其中先前的细胞聚集和结合数据要么同意,要么不同意操纵分子动力学预测。表面等离子体共振测量量化了溶液的结合特性。使用表面力仪定量粘附,该仪器先前用于研究密切相关的CD2-CD48相互作用。结果揭示了这些盐桥在平衡结合和粘附中所起的作用。我们讨论了这种行为的分子基础及其对细胞粘附的影响。
This study describes quantitative investigations of the impact of single charge mutations on equilibrium binding, kinetics, and the adhesion strength of the CD2-CD58 interaction. Previously steered molecular dynamics simulations guided the selection of the charge mutants investigated, which include the CD2 mutants D31A, K41A, K51A, and K91A. This set includes mutations in which the previous cell aggregation and binding data either agreed or disagreed with the steered molecular dynamics predictions. Surface plasmon resonance measurements quantified the solution binding properties. Adhesion was quantified with the surface force apparatus, which was used previously to study the closely related CD2-CD48 interaction. The results reveal roles that these salt bridges play in equilibrium binding and adhesion. We discuss both the molecular basis of this behavior and its implications for cell adhesion.