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. Author manuscript; available in PMC: 2014 Jan 21.
Published in final edited form as: Gut. 2011 Jan 19;60(11):1580–1588. doi: 10.1136/gut.2009.206466

Figure 5.

Figure 5

Relationship between endoplasmic reticulum (ER) stress and autophagy. Hypomorphic XBP1 function leads to ER stress and consecutive massive activation of inositol requiring enzyme-1 (IRE1), the kinase end endo-ribonuclease upstream of XBP1, along with activation of other branches of the unfolded protein response (UPR). PERK activates eIF2α and hence halts protein translation, but can also induce autophagy. JNK is phosphorylated due to overactivated IRE1 involving the adaptor TRAF2, which in turn may induce autophagy, but also apoptosis if unrestrained. Furthermore, ER stress induction per se due to hypomorphic XBP1 function may lead to autophagy induction as a compensatory mechanism.