The transcription factor c‐Jun protects against sustained hepatic endoplasmic reticulum stress thereby promoting hepatocyte survival
Matthias Fuest, Karolina Willim, Sabine MacNelly, Nicole Fellner, Guenter P. Resch, Hubert E. Blum, Peter Hasselblatt – 27 September 2011 – Endoplasmic reticulum (ER) stress due to accumulation of hepatoviral or misfolded proteins is increasingly recognized as an important step in the pathogenesis of inflammatory, toxic, and metabolic liver diseases. ER stress results in the activation of several intracellular signaling pathways including Jun N‐terminal kinase (JNK).