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. 2019 Aug 14;9(1):1–13. doi: 10.1016/j.jcmgh.2019.08.003

Figure 8.

Figure 8

Schematic of the mechanism for high ASNS expression in the pancreatic acinar cell and its up-regulation with ASNase. Heightened basal ER stress activates PERK, which in turn phosphorylates eIF2α (p-eIF2α) and activates transcription of ATF4. Binding of ATF4 on the amino acid response element of the ASNS promoter induces ASNS expression. In addition, ASNase exposure can up-regulate ASNS further through a combination of greater PERK signaling and the nutrient deprivation response through the amino acid sensor general control nonderepressible 2 (GCN2).