Fig. 8. A schematic illustration of aphidicolin-stimulated NO production and vessel relaxation. Aphidicolin activates ATM, the most upstream DNA damage sensor, followed by Akt activation. Akt in turn activates CREB that transactivates the eNOS promoter through the TRE site, resulting in increased eNOS expression. Aphidicolin simultaneously increases cellular levels of BH4, and eNOS becomes coupled. Finally, this leads to NO production that induces vessel relaxation.
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