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Putative mechanisms of BBF2H7 contribution to the UPR. BBF2H7 is weakly induced at the transcriptional level and strongly induced at the translational level during ER stress. Translated BBF2H7 is cleaved at the membrane by S1P and probably S2P in response to ER stress; its cleaved N-terminal cytoplasmic domain then translocates into the nucleus and activates transcription of ER stress resistance genes via direct binding at the CRE site.
