NorUDCA promotes degradation of α1-antitrypsin mutant Z protein by inducing autophagy through AMPK/ULK1 pathway
Fig 5
NorUDCA modulates mTOR via AMPK in HTOZ cells.
A. Western blotting analysis for phosphorylation of mTOR (Ser2448) in HTOZ cells after treatment with norUDCA for 1 hour. B. Western blotting analysis for phosphorylation of mTOR (Ser2448) in HTOZ cells after pretreatment with AICAR or compound C for 1 hour and then in the presence or absence of norUDCA for an additional 1 hour. For A and B, the lower panels are the densitometry of phospho-mTOR (Ser2448) after normalization with total mTOR. Data is expressed as mean ±SD, #<0.05 vs untreated cells, §<0.05 vs norUDCA treated cells. Total mTOR is used for normalization and GAPDH is used as a loading control. Representative is from three independent experiments. C & D. Western blotting analysis for phosphorylation of AKT in HTOZ dox+ or HTOZ dox- cells after treatment with norUDCA for 1 hour. The lower panels are the densitometry of phosphorylation of AKT after normalization with total AKT. Data is expressed as mean ± SD, #<0.05 vs no Z expression (C) or untreated cells (D). GAPDH is used as a loading control. SS is used as negative control.