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pubmed:abstractText |
In Xenopus oocytes, Ca2+ influx through an endogenous voltage-gated Ca2+ channel activates a transient outward Cl- current (ICl(Ca)), which is potentiated by cAMP increase. The site of cAMP effect appears to be the Ca2+ channel instead of the Ca(2+)-activated Cl- channel, because cAMP potentiates the Ba2+ current through the Ca2+ channel in a similar way to the ICl(Ca), and cAMP does not potentiate the Ca(2+)-dependent Cl- current in cells treated with Ca2+ ionophore. Using the catalytic subunit of protein kinase A (PKA) and PKA inhibitors, it was shown that PKA is both necessary and sufficient for the cAMP effect on ICl(Ca). Furthermore, the cAMP/PKA-mediated potentiation of ICl(Ca) was inhibited by both type 1 and type 2A protein phosphatases.
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