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Figure 3. Scheme detailing the long-term adaptive response in the livers of mutant human 
1-antitrypsin (PiZ) transgenic mice. In the endoplasmic reticulum (ER) the excess of the aggregating PiZ protein induces a shift in the function of the protein disulfide isomerase (PDI), decreasing the protein disulfide reductase activity. This is accompanied with a shift in the redox balance of the ER toward a more reduced state, a change in the ER chaperone complexes, and signs of cytoplasmic stress and antioxidant response.
