A T-type channel-calmodulin complex triggers αCaMKII activation.
A T-type channel-calmodulin complex triggers αCaMKII activation.
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DOI:
10.1186/s13041-017-0317-8
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发表时间:
2017-08-11
期刊:
影响因子:
3.6
通讯作者:
Turner RW
中科院分区:
文献类型:
--
作者:
Asmara H;Micu I;Rizwan AP;Sahu G;Simms BA;Zhang FX;Engbers JDT;Stys PK;Zamponi GW;Turner RW
Calmodulin (CaM) is an important signaling molecule that regulates a vast array of cellular functions by activating second messengers involved in cell function and plasticity. Low voltage-activated calcium channels of the Cav3 family have the important role of mediating low threshold calcium influx, but were not believed to interact with CaM. We find a constitutive association between CaM and the Cav3.1 channel at rest that is lost through an activity-dependent and Cav3.1 calcium-dependent CaM dissociation. Moreover, Cav3 calcium influx is sufficient to activate αCaMKII in the cytoplasm in a manner that depends on an intact Cav3.1 C-terminus needed to support the CaM interaction. Our findings thus establish that T-type channel calcium influx invokes a novel dynamic interaction between CaM and Cav3.1 channels to trigger a signaling cascade that leads to αCaMKII activation. The online version of this article (doi:10.1186/s13041-017-0317-8) contains supplementary material, which is available to authorized users.
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