Can Specific Protein-Lipid Interactions Stabilize an Active State of the Beta 2 Adrenergic Receptor?

Biophys J. 2015 Oct 20;109(8):1652-62. doi: 10.1016/j.bpj.2015.08.028.

Abstract

G-protein-coupled receptors are eukaryotic membrane proteins with broad biological and pharmacological relevance. Like all membrane-embedded proteins, their location and orientation are influenced by lipids, which can also impact protein function via specific interactions. Extensive simulations totaling 0.25 ms reveal a process in which phospholipids from the membrane's cytosolic leaflet enter the empty G-protein binding site of an activated β2 adrenergic receptor and form salt-bridge interactions that inhibit ionic lock formation and prolong active-state residency. Simulations of the receptor embedded in an anionic membrane show increased lipid binding, providing a molecular mechanism for the experimental observation that anionic lipids can enhance receptor activity. Conservation of the arginine component of the ionic lock among Rhodopsin-like G-protein-coupled receptors suggests that intracellular lipid ingression between receptor helices H6 and H7 may be a general mechanism for active-state stabilization.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Binding Sites
  • Carbon / chemistry
  • Humans
  • Lipid Bilayers / chemistry
  • Molecular Dynamics Simulation
  • Mutation
  • Oxygen / chemistry
  • Phosphatidylcholines / chemistry
  • Phosphatidylglycerols / chemistry
  • Protein Conformation
  • Protein Stability
  • Receptors, Adrenergic, beta-2 / genetics
  • Receptors, Adrenergic, beta-2 / metabolism*

Substances

  • Lipid Bilayers
  • Phosphatidylcholines
  • Phosphatidylglycerols
  • Receptors, Adrenergic, beta-2
  • Carbon
  • 1-palmitoyl-2-oleoylglycero-3-phosphoglycerol
  • Oxygen
  • 1-palmitoyl-2-oleoylphosphatidylcholine