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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Targeting ER stress/PKA/GSK-3β/β-catenin pathway as a potential novel strategy for hepatitis C virus-infected patients

Fig. 1

Wnt/β-catenin signaling in chronically HCV-infected Huh7.5 cells and R4-GFP HCV replicon Huh7 cells after HCV clearance by DAA which induced Wnt/β-catenin signaling and chronic HCV infection-induced PKA/GSK-3β/β-catenin signaling in HCV-infected Huh7.5 cells. A Chronic HCV-infected Huh7.5 cells (day 110) were treated with either DAA or interferon-α (IFN). After the treatment, cell lysates were collected for western blotting with indicated antibodies. UT, untreated. B R4-GFP replicon Huh7 cells were treated with DAA. After the treatment, cell lysates were collected for western blotting with indicated antibodies. Parental, Huh7 cells without HCV replicon. UT, untreated. C Uninfected Huh7.5 control cells were treated with DAA. Cell lysates were collected on day 2 and day 9 after treatment for western blotting with indicated antibodies. UT, untreated. D Chronic HCV-infected Huh7.5 cells d135, d140 and d129 were treated with mTOR inhibitor rapamycin, AKT inhibitor triciribine and PKA inhibitor H89, respectively. After 48 h, cell lysates were collected for western blotting with indicated antibodies. E Huh 7.5 cells were infected with GFP-tagged HCV. Cell lysates were taken at the indicated time points after HCV infection for western blotting with indicated antibodies

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