Hydrogen peroxide stimulation of <scp>CFTR</scp> reveals an <scp>Epac</scp>‐mediated, soluble <scp>AC</scp>‐dependent <scp>cAMP</scp> amplification pathway common to <scp>GPCR</scp> signalling

Abstract

H2 O2 initiated a complex signalling cascade that used direct stimulation of tmACs by Gαs followed by Epac-mediated Ca(2+) crosstalk to activate sAC. The Epac-mediated Ca(2+) signal constituted a positive feedback loop that amplified CFTR anion secretion following stimulation of tmAC by a variety of stimuli.