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Similarly in a mouse model of familial Alzheimer’s disease (5xFAD), impaired NVC occurred along with decreased K IR 2.1 activity (Mughal, Harraz, Gonzales, Hill-Eubanks, & Nelson, 2021)

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The first reported approach involved the utilization of a recombinant C-terminal domain of GRK2 (βARKct), comprising 195 amino acid residues (495–689 aa), including the Gβγ binding domain, which presumably serves as an inhibitor of Gβγ–GRK2 interactions