ATF6 encodes a transcription factor that is anchored in the endoplasmic reticulum (ER) and activated during the unfolded protein response (UPR) to protect cells from ER stress. Under conditions of ER stress, ATF6 is transported from the ER to the Golgi apparatus, where it is cleaved by Golgi-resident proteases to release the cytosolic DNA-binding portion. Then the processed ATF6 moves to the nucleus to activate gene expression. Deletion of the isoform activating transcription factor 6α (ATF6α) and its paralog ATF6β results in embryonic lethality and notochord dysgenesis in nonhuman vertebrates, and loss-of-function mutations in ATF6α are associated with malformed neuroretina and congenital vision loss in humans. Altered ATF6 function in neurodegenerative disorders such as Parkinson's disease has been observed.
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