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The unmodified calcitonin gene-related peptide receptor undergoes minor conformational changes upon peptide binding, triggering intracellular alterations that facilitate G protein activation.
GPR3's constitutive activity is driven by a lipid-like ligand binding in a hydrophobic groove, with conformational changes linked to receptor dynamics.
Cinacalcet and evocalcet rescued signaling in some CaSR mutants, but other activators were less effective, highlighting the need for new treatments for CaSR mutation-related disorders.
