Beta-adrenergic receptor signaling must be terminated quickly or an extended metabolic shift could cause serious problems for the organism. Which best explains how receptors are "desensitized"? A. G proteins will lead to activation of proteases, which reduces the overall amount of receptor on the cell membrane. B. Arrestin will first bind the receptor, allowing G protein-coupled receptor kinase to recognize the GPCR and phosphorylate the receptor. This increases the GTPase activity of the G protein. C. G protein-coupled receptor kinases (GRKs) are protein kinases that phosphorylate receptors for internalization. D. G protein-coupled receptor kinases (GRKs) lead to the activation of other protein kinases, which block ligand binding to the receptor binding pocket.

Question

Giovani Grimes

Biology

10 August, 01:05

Beta-adrenergic receptor signaling must be terminated quickly or an extended metabolic shift could cause serious problems for the organism. Which best explains how receptors are "desensitized"? A. G proteins will lead to activation of proteases, which reduces the overall amount of receptor on the cell membrane. B. Arrestin will first bind the receptor, allowing G protein-coupled receptor kinase to recognize the GPCR and phosphorylate the receptor. This increases the GTPase activity of the G protein. C. G protein-coupled receptor kinases (GRKs) are protein kinases that phosphorylate receptors for internalization. D. G protein-coupled receptor kinases (GRKs) lead to the activation of other protein kinases, which block ligand binding to the receptor binding pocket.

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Rihanna · Answer 1

Answer:B

Explanation:

Agonist-induced desensitization involves phosphorylation of G protein-coupled receptors by two currently recognized classes of serine/threonine protein kinases. Second messenger-dependent kinases, phosphorylating a variety of proteins, mediate a generalized cellular hyporesponsiveness termed heterologous desensitization. G protein-coupled receptor kinases (GRKs) phosphorylate specifically agonist-occupied, or activated, receptors, and thereby initiate receptor-specific, or homologous, desensitization.