B3-Adrenergic receptor is the member of GPCRs.
After agonist binding, the receptor undergoes a conformational change that induces an exchange of GDP for GTP, causing dissociation of the active Gαs and Gβγ protein subunits. The activated Gαs subunit then regulates the effector molecules downstream of the receptor. The activation of the Gαs subunit leads to activation of adenylyl cyclase, which in turn catalyzes the local conversion of ATP into cAMP. The rise in cAMP then triggers protein kinase A activation by binding to its regulatory subunits and allowing the catalytic subunit to function. Protein kinase A then acts as a nodal point and further initiates the phosphorylation of effector molecules and subsequently a functional response such as regulation of metabolism, vasodilation, and relaxation to cardiac contractility.
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