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. 2015 Mar 19;10(3):e0118743. doi: 10.1371/journal.pone.0118743

Fig 4. Exogenous expression of the EGFP-GRIP domain does not induce the dissociation of arfaptin-1 from the Golgi apparatus.

Fig 4

HeLa cells were transfected with EGFP-97-GRIP (A), EGFP-245-GRIP (B) or arfaptin-1b-AH-myc (C) for 48 h, and the cells were then stained with anti-myc and anti-golgin antibodies (anti-golgin-97, anti-golgin-245 and anti-arfaptin-1). The percentage of EGFP-GRIP- or arfaptin-1b-AH-myc-expressing cells (n>50 for each experiment) with intact Golgi marker signals was quantified, and the data are presented as the means±SDs; p<0.05 indicates significance, as determined by the unpaired Student’s t test. Scale bars, 10 μm. Asterisks indicate EGFP-97-GRIP- (A), EGFP-245-GRIP- (B) or arfaptin-1-AH-myc-expressing (C) cells. It is notable that the epitope of polyclonal goat anti-arfaptin-1 (Santa Cruz, sc19246) that was used in the current study is near the N terminus of arfaptin-1 (1a and 1b); therefore, it could not be used to detect arfaptin-1b-AH-myc because the AH domain is located in the C-terminal region of afaptin-1.