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Some variants have clear structural explanations for their loss-of-function, for example, variants can disrupt binding of carnitine (R471C/H/P), affect the Na + -binding site (N32S), disrupt the TM2-TM11 H-bonding network (S467C) or perturb gating residues conserved in OCTs/OATs (R169Q/P/W)

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It has been shown that NBD treatment results in a decrease in tumor growth rate in mouse and human glioblastoma models and extends survival time from 30 to 50 days in mice

[37] [38] Although TAAR1 is implicated in amphetamine-induced transporter phosphorylation, the magnitude of TAAR1-mediated monoamine release in humans remains unclear