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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Ca2+-dependent endoplasmic reticulum stress correlation with astrogliosis involves upregulation of KCa3.1 and inhibition of AKT/mTOR signaling

Fig. 5

AKT modulation is crucial for KCa3.1-mediated ER stress in astrocytes. a Representative blots of p-AKT and total AKT from the hippocampi of postmortem human AD patients and age-matched controls. b Data are presented as the mean ± SEM (n = 3–5). The OD value of p-AKT was normalized to that of AKT. **p < 0.01 vs. control brains (unpaired, two-tailed Student’s t test). c Representative images of p-AKT and total AKT in KCa3.1−/− astrocytes, responses to 5 μM Aβ 1 h vs. WT cells. d Mean values of p-AKT relative to AKT. Data are presented as the mean ± SEM (n = 3). *p < 0.05, **p < 0.01 vs. controls (one-way ANOVA followed by the Dunnett’s multiple comparison test). e Brain tissues from 15-month-old WT, KCa3.1−/−, APP/PS1, and KCa3.1−/−/APP/PS1 mice were subjected to SDS-PAGE, and immunoblotted with antibodies against p-AKT, total AKT, p-mTOR, total mTOR, p-4EBP1, and p-p70 S6. f Data are presented as the mean ± SEM (n = 4). The OD values of p-AKT and p-mTOR were normalized to those of AKT and mTOR, respectively. The OD values of p-4EBP1 and p-p70 S6 were normalized to that of β-actin. *p < 0.05, **p < 0.01 (one-way ANOVA followed by the Dunnett’s multiple comparison test). Con control, WT wild-type

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