Hepatocytic p62 suppresses ductular reaction and tumorigenesis in mouse livers with mTORC1 activation and defective autophagy
Background & Aims Either activation of mTORC1 due to loss of Tsc1 (tuberous sclerosis
complex 1) or defective hepatic autophagy due to loss of Atg5 leads to spontaneous liver
tumorigenesis in mice. The purpose of this study was to investigate the mechanisms by
which autophagy contributes to the hepatic metabolic changes and tumorigenesis mediated
by mTORC1 activation. Methods Atg5 Flox/Flox (Atg5 F/F) and Tsc1 F/F mice were crossed
with albumin-Cre mice to generate liver-specific Atg5 knockout (L-Atg5 KO), L-Tsc1 KO and …
complex 1) or defective hepatic autophagy due to loss of Atg5 leads to spontaneous liver
tumorigenesis in mice. The purpose of this study was to investigate the mechanisms by
which autophagy contributes to the hepatic metabolic changes and tumorigenesis mediated
by mTORC1 activation. Methods Atg5 Flox/Flox (Atg5 F/F) and Tsc1 F/F mice were crossed
with albumin-Cre mice to generate liver-specific Atg5 knockout (L-Atg5 KO), L-Tsc1 KO and …