et al., 2013), 5-HT receptors (Joubert et al., 2004), multidrug resistance-associated protein 4 (Hayashi et al., 2012) and β2 adrenergic receptors (Lauffer et al., 2010). For β2 adrenergic receptors, knockdown of SNX27 by RNAi in cultured aortic smooth muscle cells decreases forward trafficking of β2 adrenergic receptors, leading to reduced adrenergic signaling (Lauffer et al., 2010). How endogenously expressed SNX27 regulates GIRK channel expression in vivo remains an important but unanswered question. Mice with a complete SNX27 null mutation, however, exhibit severe developmental defects and die postnatally (Cai et al., 2011), precluding assessment of SNX27 on GIRK function in vivo. Heterozygote SNX27+/− mice, on the other hand, appear to have normal neurodevelopment but exhibit defects in excitatory neurotransmission in the hippocampus, due to reduced levels of AMPA and NMDA receptors (Wang et al., 2013).
