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-Abl complex communicates ER stress to the mitochondria – an essential step in subsequent apoptosisFiles in this Data Supplement:
Fig. S1. Effects of treatment of δV1-1 on ER-stress-related apoptotic molecules CHOP and caspase12. (A) Rats were subjected to 2 hours middle cerebral artery occlusion (MCAO) followed by 24 hours of re-perfusion (I/R). δV1-1 and TAT control (0.2 mg/kg) were injected intraperitoneally at the onset of reperfusion. CHOP and pro-caspase 12 were detected by western blot analysis. GAPDH was used as internal loading control. Data are expressed as mean ± s.e. of six rats in each group. *P<0.05 vs TAT treatment; #P<0.05 vs sham operated rats. Neuro2a cells were pre-treated with δV1-1 or TAT control (1 µM) for 15 minutes followed b treatment with (B) tunicamycin (Tm; 5 µg/ml) or (C) thapsigargin (Tg; 3 µM). After 24 hours stimulation, CHOP and pro-caspase 12 were detected in total lysates by western blot analysis. GAPDH was used as internal loading control.
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