Specifically, mutagenesis of ECD, ECL1 and ECL3 individually increased the basal activity of GCGR, which could result from the interruption of intramolecular interactions between the ECD and ECL1/3 that otherwise stabilize the receptor in an inactive state
doi:10.1001/jama.2023.2438 5
Treatment should begin immediately without waiting for laboratory confirmation, since delays can result in irreversible neurologic injury
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