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Therefore, the major oxidative burst during I/R occurs after the reexposure to oxygen during the so called warm ischemia time.7 Although the molecular mechanisms involved in I/R cellular responses are still not fully understood, a major role seems to be played by APE/Ref-1 and NF-B proteins in liver.42 Overexpression of APE/Ref-1 by adenoviral vector resulted in suppression of the reperfusion-generated oxidative stress in a mouse model.42 Liver transplantation (LT) is at present the only available choice for the treatment of end-stage hepatic disease

OsMADS23 interacts with the SnRK2-type protein kinase SAPK9, which phosphorylates it, increasing its stability and transcriptional activity

Lung Cancer 74 (3), 481485

Under mild oxidative stress, induction of GSTP1-1 expression and its redox recycling function afford cellular protection