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Fig. 7 | Molecular Medicine

Fig. 7

From: iNOS/NO is required for IRF1 activation in response to liver ischemia-reperfusion in mice

Fig. 7

Schematic of the proposed model of iNOS/NO-mediated IRF1 activation in response to hepatic I/R in mice. Ischemia and reperfusion induces iNOS/NO, which activates IRF1 transcriptional activities. This process requires iNOS/NO induced HDAC2 activation to catalyze deacetylation of histone H3. On the other hand, iNOS gene deficiency decreases IRF1 and HDAC2 activities. The activated IRF1 as a transcription factor is translocated into the nucleus, where it regulates transcription of the target genes associated with cell death and cell cycle repression such as, iNOS, PUMA and p21. A positive feedback loop between IRF1 and iNOS may lead to IRF1 continuatively activated. Inhibition of HDAC2 by its inhibitor leads to an increase in histone H3 acetylation, and a decrease in IRF1 nuclear translocation and its target gene expressions (see Results and Discussion). I/R induced IRF1 activation requires iNOS/NO, which recruits HDAC2 as a co-activator to mediate chromatin modification

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