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Analogously to the S168R and S217R human GnRHR mutants, the V 2 Rs with amino acid exchanges at the TMD2 and TMD4 interface (H80R, W164R, and S167L mutants) also showed recalcitrance to pharmacoperone treatment, most probably due to the severity of the folding defect as a consequence of the nature of the amino acid replacement (111, 195)

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Altered connectivity in depression: GABA and glutamate neurotransmitter deficits and reversal by novel treatments