IndraLab

Statements



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"Basolateral UDP induced a sustained activation of Cl (-) secretion, which was completely inhibited by 293B, a specific inhibitor of cAMP stimulated basolateral KCNQ1 and KCNE3 K (+) channels."

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"In RNF5WT and CFTRWT animals, addition of the cAMP elevating agent forskolin to the serosal side of tissue induces a negative shift in transepithelial potential difference (and therefore in the equivalent short-circuit current) reportedly due to cAMP dependent activation of the apical CFTR and of the basolateral potassium channel KCNQ1 and KCNE3, which enables recycling of potassium through the basolateral membrane and maintenance of membrane potential favorable to chloride efflux (XREF_FIG)."

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"Mall et al. demonstrated that activation of the cAMP pathway increased CaCC mediated secretion in cystic fibrosis and, conversely, chromanol 293B, an inhibitor of cAMP activated Kv7.1 channels was able to fully abolish nucleotide activated Cl- secretion (Mall et al., 2003)."

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"Further, at least two KCNE1 mutations linked to LQT-5 (D76N and W87R) cause functional disruption of cAMP mediated KCNQ1 and KCNE1-channel regulation despite the response of the substrate protein (KCNQ1) to protein kinase A phosphorylation."