Chen Y, Pollock J D, Wang Y, DePaoli-Roach A A, Yu L
Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis 46202.
FEBS Lett. 1993 Dec 27;336(2):191-6. doi: 10.1016/0014-5793(93)80800-a.
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.
在非洲爪蟾卵母细胞中，通过内源性电压门控钙通道的Ca2+内流激活了一个短暂的外向Cl-电流（ICl(Ca)），该电流会因cAMP增加而增强。cAMP作用的位点似乎是钙通道而非Ca(2+)激活的Cl-通道，因为cAMP以类似于ICl(Ca)的方式增强通过钙通道的Ba2+电流，并且cAMP不会增强用Ca2+离子载体处理的细胞中Ca(2+)依赖性Cl-电流。使用蛋白激酶A（PKA）的催化亚基和PKA抑制剂表明，PKA对于cAMP对ICl(Ca)的作用既必要又充分。此外，ICl(Ca)的cAMP/PKA介导的增强作用受到1型和2A型蛋白磷酸酶的抑制。
