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. 2017 Jan 20;19(1):43–53. doi: 10.1016/j.neo.2016.11.007

Figure 3.

Figure 3

Overexpression of GRP78 drives Golgi-to-ER relocation of GALNT6. Immunocytochemistry was performed in the HeLa-Mock and -GALNT6-WT stable cells. (A) Forty-eight hours after transfection of Flag-tagged GRP78 expression vectors into the HeLa stable cells, immunocytochemistry was performed by using anti-Flag and anti-HA antibodies. Flag-tagged GRP78 was shown in green color and HA-tagged GALNT6 was in red color. We observed that HA-tagged GALNT6 located in Golgi if exogenous GRP78 was not expressed (yellow arrows), but a large amount of Flag-tagged GRP78 drove Golgi-to-ER relocation of GALNT6 in the HeLa-GALNT6-WT stable cells (white arrows). Two fields were taken for each condition. (B) The HeLa stable cells were treated with DMSO (control) or 2 μM of an ER stress activator TG for 4 h, and immunocytochemistry was performed by using anti-GRP78 and anti-HA antibodies. Endogenous GRP78 was shown in green color and HA-tagged GALNT6 was in red color. After ER stress by TG treatment, endogenous expression of GRP78 was significantly increased, and drove Golgi-to-ER relocation of GALNT6. Three fields were taken for TG-treated HeLa-GALNT6-WT stable cells.