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Schematic model for ER stress and UPR activation
In the ER “Zen” status, the ER maintains protein and Ca2+ homeostasis. In the ER “Stress” status, accumulation of misfolded proteins induces the release of BiP from PERK, IRE1α and ATF6. These arms can be subsequently activated in a signaling cascade termed the UPR, which involves the downregulation of translation and the activation of transcription factors that regulate target genes to promote ER homeostasis and cell survival
