Advertisement

 

 

A T-type channel-calmodulin complex triggers αCaMKII activation.

A T-type channel-calmodulin complex triggers αCaMKII activation.
Author Information (click to view)

Asmara H, Micu I, Rizwan AP, Sahu G, Simms BA, Zhang FX, Engbers JDT, Stys PK, Zamponi GW, Turner RW,


Asmara H, Micu I, Rizwan AP, Sahu G, Simms BA, Zhang FX, Engbers JDT, Stys PK, Zamponi GW, Turner RW, (click to view)

Asmara H, Micu I, Rizwan AP, Sahu G, Simms BA, Zhang FX, Engbers JDT, Stys PK, Zamponi GW, Turner RW,

Advertisement

Molecular brain 2017 08 1110(1) 37 doi 10.1186/s13041-017-0317-8
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.

Submit a Comment

Your email address will not be published. Required fields are marked *

twenty − 3 =

[ HIDE/SHOW ]