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In addition to the PERK-ATF4-CHOP axis, other key ER stress pathways, such as IRE1/XBP1 and ATF6 also contribute to the UPR, collectively managing protein misfolding and restoring homeostasis, or, if stress persists, trigger cell death ( Various studies targeting ER stress signaling pathways and components of the UPR have demonstrated that CHAC1 expression is upregulated downstream of the ATF4-dependent signaling pathway (Figure 4)

Shen and Shi 2015)