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This finding reveals a novel mechanism involving a functional RA domain and interaction with Ras-like G proteins in modulating SNX27b′s control of GIRK channel surface expression and cellular excitability ( SNX27 is crucial for maintaining GIRK currents in both the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) DA neurons (Rifkin et al., 2018)
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