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. Author manuscript; available in PMC: 2012 Dec 15.
Published in final edited form as: Free Radic Biol Med. 2011 Sep 16;51(12):2172–2184. doi: 10.1016/j.freeradbiomed.2011.09.005

Fig. 3. Effect of ER stress on ER protein markers, protein/mitochondrial damage, level of pro-apoptotic protein and cell survival.

Fig. 3

ER stress was induced with in vivo thapsigargin (3 mg/kg, i.p. for 48 hrs) prior to assessment of ER stress, protein carbonyl formation, cell survival, mitochondrial aconitase activity and the pro-apoptotic protein BAD in WT and MyAkt mouse hearts. A: Gadd153 expression; B: GRP78 expression; C: phosphor-eIF2α (peIF2α) expression; D: Protein carbonyl levels; E: Cell survival using MTT assay; F: Aconitase activity. G: BAD expression; H: pBAD expression; and I: pBAD-to-BAD ratio. Insets: Representative gel blots depicting Gadd153, GRP78, peIF2α, BAD and pBAD using specific antibodies (β-actin was used as the loading control); Mean ± SEM, n = 5–7 hearts per group, * p < 0.05 vs. WT group, # p < 0.05 vs. WT-Thapsigargin (TG) group.