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. Author manuscript; available in PMC: 2021 Mar 1.
Published in final edited form as: FEBS Lett. 2019 Nov 30;594(6):1088–1100. doi: 10.1002/1873-3468.13685

Figure 4. ER stress induced cell surface localization of GRP78 and Akt signaling is reduced in GIV depleted cells.

Figure 4.

A. Scr-shRNA and GIV-shRNA cells were treated with tunicamycin or DMSO for 6h following which the cell surface proteins were biotinylated and separated from the non-biotinylated fraction through affinity purification using the streptavidin-agarose resin. The biotinylated (cell surface proteins) and flow-through (intracellular) fractions were then analyzed by immunoblotting. EGFR served as a cell surface protein control, and GAPDH as an intracellular protein control. B. The % cell surface localization of GRP78 was calculated by densitometric analysis. The Scr control was plotted to 100% and the relative % localization in GIV-shRNA cells was calculated. n=3. Errors bars represent ± S.E.M. *p <0.05. C. and D. Scr-shRNA and GIV-shRNA cells were ER stressed using tunicamycin for the indicated time-points before lysis. The cell lysates were analyzed by immunoblotting.