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These data indicate that the intracellular end of M3 and the M1–M2 linker of β2 modulate desensitization, conceivably via an intersubunit (α–β) interaction, which is consistent with the close proximity of α1 M3 C-terminal end to the M1–M2 linker of an adjacent β2 subunit, as seen in our structural models (see below)

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