Fig. 6: Sestrin2 attenuates bile acid-induced ER stress via an AMPK/mTORC1-dependent mechanism.

A, B HepG2 cells were infected with sh-SESN2 lentivirus and treated with 200 µM CDCA or 750 µM CA for the indicated times in the presence or absence of 100 µM AICAR. Cell lysates were immunoblotted with the indicated antibodies. C, D HepG2 cells were infected with sh-SESN2 lentivirus and treated with 200 µM CDCA or 750 µM CA for 9 h in the presence or absence of 100 nM rapamycin (Rap). Cell lysates were immunoblotted with the indicated antibodies. E HepG2 cells were infected with sh-Luc or sh-TSC2 lentiviruses and treated with 200 µM CDCA for the indicated times. Cell lysates were immunoblotted with the indicated antibodies. β-Actin served as a loading control. Numbers below the immunoblot bands indicate the fold changes normalized to the control band intensities. The data are representative of at least three independent experiments.