Fig. 8.

Proposed model of a role of TMEM33 in regulation of the PERK and IRE1α axes of the unfolded protein response signaling. ER stress leads to increased expression of TMEM33 and activation of PERK resulting in enhanced levels of p-eIF2α and ATF4. Depending of the cell type, overexpression of TMEM33 may also increase expression of p-IRE1α and its effector XBP1-S. Additional downstream effectors include increased expression of CHOP, cleaved caspase-7, cleaved PARP, and autophagosome marker LC3II, and reduced expression of p62. Dashed arrows indicate as yet unknown pathways