Title |
A T-type channel-calmodulin complex triggers αCaMKII activation
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Published in |
Molecular Brain, August 2017
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DOI | 10.1186/s13041-017-0317-8 |
Pubmed ID | |
Authors |
Hadhimulya Asmara, Ileana Micu, Arsalan P. Rizwan, Giriraj Sahu, Brett A. Simms, Fang-Xiong Zhang, Jordan D. T. Engbers, Peter K. Stys, Gerald W. Zamponi, Ray W. Turner |
Abstract |
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. |
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Student > Master | 2 | 9% |
Lecturer | 1 | 5% |
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Pharmacology, Toxicology and Pharmaceutical Science | 1 | 5% |
Other | 2 | 9% |
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