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Suggested causes and mechanisms include immune-mediated responses, altered drug metabolism associated with glutathione deficiency or slow acetylator phenotype, co-existing infections with cytomegalovirus (CMV) or Epstein-Barr virus (EBV), or cytokines involvement

We observe a hydrophobic extracellular gate directly above the substrate-binding site, similar to that seen in OCT1, where residues of gating helices TM1 and TM7 pack together in both the occluded and inward conformations (e.g

[231] when triggered by amphetamine, this pathway activates Ras homolog A (RhoA) and its downstream protein kinase, Rho-associated coiled-coil kinase (ROCK), an effect that internalizes both DAT and the neuronal glutamate transporter EAAT3

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