G protein-coupled receptors

(noun)

These comprise a large protein family of transmembrane receptors that sense molecules outside the cell and activate inside signal transduction pathways and, ultimately, cellular responses. Any adrenergic effects on cells are generally mediated by G protein-coupled receptors.

Related Terms

Examples of G protein-coupled receptors in the following topics:

  • Ionotropic and Metabotropic Receptors

    • Although both ionotropic and metabotropic receptors are activated by neurotransmitters, ionotropic receptors are channel-linked while metabotropic receptors initiate a cascade of molecules via G-proteins.
    • Two types of membrane-bound receptors are activated with the binding of neurotransmitters: ligand-gated ion channels (LGICs) inotropic receptors and metabotropic G- protein coupled receptors.
    • Metabotropic receptors are a subtype of membrane receptors that do not form an ion channel pore but use signal transduction mechanisms, often G proteins, to activate a series of intracellular events using second messenger chemicals.
    • The metabotropic G protein-coupled receptors have seven hydrophobic transmembrane domains.
    • When the neurotransmitter binds to the receptor, there is an activation via the G-protein that later activates the  secondary messengers.

  • Adrenergic Neurons and Receptors

    • The adrenergic receptors (or adrenoceptors) are a class of metabotropic G protein-coupled receptors that are targets of the catecholamines, especially norepinephrine or noradrenaline, and epinephrine (adrenaline).
    • There are two main groups of adrenergic receptors, α and β, with several subtypes. α receptors have the subtypes α1 (a Gq coupled receptor) and α2 (a Gi coupled receptor).
    • All three are linked to Gs proteins (although β2 also couples to Gi), which in turn are linked to adenylate cyclase.
    • α1-adrenergic receptors are members of the G protein-coupled receptor superfamily.
    • On activation, a heterotrimeric G protein, Gq, activates phospholipase C (PLC).

  • Direct Gene Activation and the Second-Messenger System

    • Most hormone receptors are G protein-coupled receptors.
    • Upon hormone binding, the receptor undergoes a conformational change and exposes a binding site for a G-protein.
    • The G-protein is bound to the inner membrane of the cell and consists of three sub-units: alpha, beta, and gamma.
    • Upon binding to the receptor, it releases a GTP molecule, at which point the alpha sub-unit of the G-protein breaks free from the beta and gamma sub-units and is able to move along the inner membrane until it contacts another membrane-bound protein: the primary effector. 
    • G-protein is activated and produces an effector. 3.

  • Agonists, Antagonists, and Drugs

    • Acetylcholine receptor agonists and antagonists can have a direct effect on the receptors or exert their effects indirectly.
    • Muscarinic receptors are coupled to the Gi-protein; therefore, vagal activation decreases cAMP.
    • Gi-protein activation also leads to the activation of KACh channels that increase potassium efflux and hyperpolarizes the cells.
    • Muscarinic receptor antagonists bind to muscarinic receptors, thereby preventing ACh from binding to and activating the receptor.
    • Nicotinic acetylcholine receptors are receptors found in the central nervous system, the peripheral nervous systems, and skeletal muscles.

  • Peripheral Motor Endings

    • Acetylcholine diffuses into the synaptic cleft and binds to the nicotinic acetylcholine receptors located on the motor end plate.
    • This depolarization spreads across the surface of the muscle fiber and continues the excitation–contraction coupling to contract the muscle.
    • The depolarization activates L-type, voltage-dependent calcium channels (dihydropyridine receptors) in the T-tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum.
    • As intracellular calcium levels rise, the motor proteins responsible for the contractile response are able to interact, as shown in Figure 3, to form cross-bridges and undergo shortening.
    • Detailed view of a neuromuscular junction: 1) Presynaptic terminal; 2) Sarcolemma; 3) Synaptic vesicle; 4) Nicotinic acetylcholine receptor; 5) Mitochondrion.

  • Antigen-Presenting Cells

    • These professional APCs are equipped with special immunostimulatory receptors that allow for enhanced activation of T cells.
    • This maturation process is dependent on signaling from other pathogen-associated molecular pattern (PAMP) molecules through pattern recognition receptors, such as the members of the Toll-like receptor family.
    • The DC uses lysosome-associated enzymes to digest pathogen-associated proteins into smaller peptides.
    • In the lymph node, the DC will display these antigenic peptides on its surface by coupling them to MHC Class II molecules.
    • In the upper pathway; foreign protein or antigen (1) is taken up by an antigen-presenting cell (2).

  • Ion Channels

    • Ion channels are membrane proteins that allow ions to travel into or out of a cell.
    • Plasma membrane is studded with a variety of membrane proteins that act as ion channels.
    • A large subset function as neurotransmitter receptors—they occur at postsynaptic sites, and the chemical ligand that gates them is released by the presynaptic axon terminal.
    • Ligand-gated ion channels (LGICs) are one type of ionotropic receptor or channel-linked receptor.
    • Example of primary active transport, where energy from hydrolysis of ATP is directly coupled to the movement of a specific substance across a membrane independent of any other species.

  • Cephalic Phase

    • There will also be an influence on G cells to increase gastrin circulation.
    • When food enters stomach, the stomach stretches and activates stretch receptors.
    • Receptors send message to the medulla, and then back to the stomach via the vagus nerve.
    • Chemical stimuli (i.e., partially digested proteins, caffeine) directly activate G-cells (enteroendocrine cells) located in the pyloric region of the stomach to secrete gastrin; this in turn stimulates gastric glands to secrete gastric juice.

  • Microbial Evasion of Phagocytosis

    • First, they grow in sites that phagocytes are not capable of traveling to (e.g. the surface of unbroken skin).
    • Bacteria often produce proteins or sugars that coat their cells and interfere with phagocytosis; these are called capsules.
    • Streptococcus pneumoniae produces several types of capsule which provide different levels of protection, and group A streptococci produce proteins such as M protein and fimbrial proteins to block engulfment.
    • Some proteins hinder opsonin-related ingestion.
    • Staphylococcus aureus produces Protein A to block antibody receptors, which decreases the effectiveness of opsonins.

  • Structure and Function of Antibodies

    • An antibody is a Y-shaped protein that is produced by B cells to identify and neutralize antigens in the body.
    • IgD: Functions mainly as an antigen receptor on B cells that have not been exposed to antigens.
    • This is because it expresses a tail for Fc receptors on phagocytes to bind to, which activates phagocytosis.
    • Eliminates pathogens in the early stages of B cell mediated (humoral) immunity before there is sufficient IgG.
    • Like IgG, it can also activate the classical complement system.