Transcriptional regulator that acts as a mediator of the integrated stress response (ISR) through transcriptional control of protein homeostasis under conditions of ER stress (PubMed:33384352). Controls the outcome of the unfolded protein response (UPR), an ER-stress response pathway that either promotes recovery of ER homeostasis and cell survival, or triggers the terminal UPR which elicits programmed cell death when ER stress is prolonged and unresolved (PubMed:33384352). ER stress induces QRICH1 translation by a ribosome translation re-initiation mechanism in response to EIF2S1/eIF-2-alpha phosphorylation, and stress-induced QRICH1 regulates a transcriptional program associated with protein translation, protein secretion-mediated proteotoxicity and cell death during the terminal UPR (By similarity). May cooperate with ATF4 transcription factor signaling to regulate ER homeostasis which is critical for cell viability (By similarity). Up-regulates CASP3/caspase-3 activity in epithelial cells under ER stress. Central regulator of proteotoxicity associated with ER stress-mediated inflammatory diseases in the intestines and liver (PubMed:33384352). Involved in chondrocyte hypertrophy, a process required for normal longitudinal bone growth (PubMed:30281152). Expressed highly in prefrontal cortex, craniofacial area and near the limbs of mouse embryos. Expressed in heart, skeletal muscle, liver, kidney, lung, brain, spleen, intestine and growth plate in mice. The CARD domain may be involved in the regulation of caspase activity in the context of programmed cell death.