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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: Biochim Biophys Acta. 2012 Dec 13;1833(3):686–697. doi: 10.1016/j.bbamcr.2012.12.004

FIGURE 5. Regulation of the influx of acetyl-CoA into the ER lumen as part of the UPR.

FIGURE 5

The constant influx of acetyl-CoA into the ER lumen is required to control the induction of autophagy/ERAD(II) as part of the UPR. Specifically, AT-1 acts downstream of IRE1/XBP1 signaling. If the influx of acetyl-CoA is maintained, ERAD(II) helps to eliminate unwanted unfolded/misfolded aggregates without inducing cell death (A). However, if the influx is not maintained, programmed Type II (autophagic) cell death is activated (B). The autophagy protein Atg9A seems to act as a “sensor” for the acetylation status of the ER.