Abstract
G-protein coupled receptors (GPCRs) are membrane proteins that convey extracellular signals to the cellular milieu. They represent a target for more than 30% of currently marketed drugs. Here we review the effects of membrane cholesterol on the function of GPCRs of Class A. We review both the specific effects of cholesterol mediated via its direct high-affinity binding to the receptor and non-specific effects mediated by cholesterol-induced changes in the properties of the membrane. Cholesterol binds to many GPCRs at both canonical and non-canonical binding sites. It allosterically affects ligand binding to and activation of GPCRs. Additionally, it changes the oligomerization state of GPCRs. In this review, we consider a perspective of the potential for the development of new therapies that are targeted at manipulating the level of membrane cholesterol or modulating cholesterol binding sites on to GPCRs.
Highlights
G-protein coupled receptors (GPCRs) are membrane proteins that pass on extracellular signals to the cell using heterotrimeric GTP-binding proteins (G-proteins)
Other non-structural functions of CLR include its physical interaction with many modulation of membrane cholesterol and modulation of CLR-binding sites as potential membrane proteins including GPCRs (Figure 1B)
The results suggest that the energy landscape of CLR association with GPCRs corresponds to a series of shallow minima separated by low barriers
Summary
G-protein coupled receptors (GPCRs) are membrane proteins that pass on extracellular signals to the cell using heterotrimeric GTP-binding proteins (G-proteins). Non-structural functions of CLR include its physical interaction with many pending on theOther distribution of the receptor subtypes in the body This interaction results inthe alteration of agent to target body organs selectively, it has to be able to differentially influence acreceptor properties in terms of theIn processes binding, tivation of individual receptor subtypes. Membrane can be considered an allosteric nous signalling molecule is conserved among its receptor subtypes This is necessarymodulator for of GPCRs possessing its own specific allosteric binding site. Other non-structural functions of CLR include its physical interaction with many modulation of membrane cholesterol and modulation of CLR-binding sites as potential membrane proteins including GPCRs (Figure 1B) This interaction results in alteration of therapeutic targets.
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