A T-type channel-calmodulin complex triggers αCaMKII activation
| dc.contributor.author | Asmara, Hadhimulya | |
| dc.contributor.author | Micu, Ileana | |
| dc.contributor.author | Rizwan, Arsalan P | |
| dc.contributor.author | Sahu, Giriraj | |
| dc.contributor.author | Simms, Brett A | |
| dc.contributor.author | Zhang, Fang-Xiong | |
| dc.contributor.author | Engbers, Jordan D T | |
| dc.contributor.author | Stys, Peter K | |
| dc.contributor.author | Zamponi, Gerald W | |
| dc.contributor.author | Turner, Ray W | |
| dc.date.accessioned | 2018-09-26T12:09:45Z | |
| dc.date.available | 2018-09-26T12:09:45Z | |
| dc.date.issued | 2017-08-11 | |
| dc.date.updated | 2018-09-26T12:09:44Z | |
| dc.description.abstract | 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. | |
| dc.identifier.citation | Molecular Brain. 2017 Aug 11;10(1):37 | |
| dc.identifier.doi | https://doi.org/10.1186/s13041-017-0317-8 | |
| dc.identifier.uri | http://hdl.handle.net/1880/108005 | |
| dc.language.rfc3066 | en | |
| dc.rights.holder | The Author(s). | |
| dc.title | A T-type channel-calmodulin complex triggers αCaMKII activation | |
| dc.type | Journal Article |