A T-type channel-calmodulin complex triggers alpha CaMKII activation

作者：Asmara Hadhimulya; Micu Ileana; Rizwan Arsalan P; Sahu Giriraj; Simms Brett A; Zhang Fang Xiong; Engbers Jordan D T; Stys Peter K; Zamponi Gerald W; Turner Ray W^*

来源：Molecular Brain, 2017, 10(1): 37.

DOI：10.1186/s13041-017-0317-8

• Calmodulin
• Cav3.1
• T-type channel
• alpha CaMKII
• Hippocampus
• Purkinje cell
• Cerebellum

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 alpha CaMKII 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 alpha CaMKII activation.

• 出版日期2017-8-11