Hedger George, Shorthouse David, Koldsø Heidi, Sansom Mark S P
Department of Biochemistry, University of Oxford , South Parks Road, Oxford OX1 3QU, United Kingdom.
MRC Cancer Unit, University of Cambridge , MRC Research Centre, Box 197, Cambridge CB2 0X1, United Kingdom.
J Phys Chem B. 2016 Aug 25;120(33):8154-63. doi: 10.1021/acs.jpcb.6b01387. Epub 2016 May 9.
Lipid molecules can bind to specific sites on integral membrane proteins, modulating their structure and function. We have undertaken coarse-grained simulations to calculate free energy profiles for glycolipids and phospholipids interacting with modulatory sites on the transmembrane helix dimer of the EGF receptor within a lipid bilayer environment. We identify lipid interaction sites at each end of the transmembrane domain and compute interaction free energy profiles for lipids with these sites. Interaction free energies ranged from ca. -40 to -4 kJ/mol for different lipid species. Those lipids (glycolipid GM3 and phosphoinositide PIP2) known to modulate EGFR function exhibit the strongest binding to interaction sites on the EGFR, and we are able to reproduce the preference for interaction with GM3 over other glycolipids suggested by experiment. Mutation of amino acid residues essential for EGFR function reduce the binding free energy of these key lipid species. The residues interacting with the lipids in the simulations are in agreement with those suggested by experimental (mutational) studies. This approach provides a generalizable tool for characterizing the interactions of lipids that bind to specific sites on integral membrane proteins.
脂质分子可与整合膜蛋白上的特定位点结合,从而调节其结构和功能。我们进行了粗粒度模拟,以计算糖脂和磷脂在脂质双层环境中与表皮生长因子受体跨膜螺旋二聚体上的调节位点相互作用时的自由能分布。我们确定了跨膜结构域两端的脂质相互作用位点,并计算了脂质与这些位点的相互作用自由能分布。不同脂质种类的相互作用自由能范围约为-40至-4 kJ/mol。那些已知可调节表皮生长因子受体功能的脂质(糖脂GM3和磷酸肌醇PIP2)与表皮生长因子受体上的相互作用位点表现出最强的结合,并且我们能够重现实验所表明的GM3相对于其他糖脂在相互作用上的偏好。表皮生长因子受体功能所必需的氨基酸残基的突变会降低这些关键脂质种类的结合自由能。模拟中与脂质相互作用的残基与实验(突变)研究提出的残基一致。这种方法为表征与整合膜蛋白上特定位点结合的脂质的相互作用提供了一种可推广的工具。