
Replacement of endogenous SNX1 with wild-type SNX1 rescues normal trafficking of mGluR1. A, B, Western blot (A) and quantitation of the Western blots (B), showing the efficient knock-down of endogenous SNX1 by shSNX1 and replacement of the endogenous SNX1 with full-length SNX1. C, Representative cells showing that knockdown of endogenous SNX1 with shSNX1 and expression of the wild-type SNX1 replacement construct had no effect on the surface expression of myc-mGluR1. D, Quantitation of surface myc-mGluR1 following knockdown and replacement of endogenous SNX1. E, Representative examples of surface and internalized myc-mGluR1, 30 min after 100 μm R,S-DHPG application in control cells, shSNX1-expressing cells, shSNX1 and wild-type SNX1-expressing cells. F, Quantitation suggested that knockdown of endogenous SNX1 resulted in the rapid recycling of myc-mGluR1 and expression of wild-type SNX1 rescued the normal trafficking of the receptor. Results are presented as mean ± SEM collected from three independent experiments. Scale bar, 10 μm. ***p < 0.001, *p < 0.05; n.s., p > 0.05.




