Under conditions of ER stress, PERK undergoes autophosphorylation and activates its kinase activity. This activation leads to the phosphorylation of the eukaryotic initiation factor 2α (eIF2α), which reduces the rate of global protein synthesis, thereby decreasing the protein load on the ER. Additionally, this phosphorylation event selectively promotes the translation of specific stress-related proteins, such as ATF4, which helps in cellular adaptation and survival.
