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In both types of cells, upon ER stress induction by thapsigargin (Tg) treatment, all the three UPR pathways were activated, as determined by phosphorylation of IRE1α, PERK, eIF2α, and cleavage of ATF6 to generate the activated form, as well as increased expression of the downstream transcription factors XBP1s and ATF4 (Fig
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