Molecular mechanism of TMEM16A regulation: role of CaMKII and PP1/PP2A
Molecular mechanism of TMEM16A regulation: role of CaMKII and PP1/PP2A
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DOI：
10.1152/ajpcell.00059.2018
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发表时间：
2019-12-01
影响因子：
5.5
通讯作者：
Leblanc, Normand
中科院分区：
文献类型：
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作者：
Ayon, Ramon J.;Hawn, Matthew B.;Leblanc, Normand
本研究探讨了Tmem 16 a基因编码的钙激活氯离子通道（CaCCs）受钙调蛋白依赖性蛋白激酶II（CaMKII）和蛋白磷酸酶1（PP 1）和2A（PP 2A）调控的机制。从表达小鼠TMEM 16 A的HEK-293细胞记录Ca 2+激活的Cl-电流（I-ClCa）。在存在（5 mM）或不存在ATP的情况下，使用移液管溶液诱发I-ClCa，其中游离Ca 2+浓度被夹持至500 nM。在5 mM ATP的情况下，I-ClCa衰减至
This study explored the mechanism by which Ca2+-activated Cl- channels (CaCCs) encoded by the Tmem16a gene are regulated by calmodulin-dependent protein kinase II (CaMKII) and protein phosphatases 1 (PP1) and 2A (PP2A). Ca2+-activated Cl- currents (I-ClCa) were recorded from HEK-293 cells expressing mouse TMEM16A. I-ClCa were evoked using a pipette solution in which free Ca2+ concentration was clamped to 500 nM, in the presence (5 mM) or absence of ATP. With 5 mM ATP, I-ClCa decayed to