A T-type channel-calmodulin complex triggers αCaMKII activation

dc.contributor.authorAsmara, Hadhimulya
dc.contributor.authorMicu, Ileana
dc.contributor.authorRizwan, Arsalan P
dc.contributor.authorSahu, Giriraj
dc.contributor.authorSimms, Brett A
dc.contributor.authorZhang, Fang-Xiong
dc.contributor.authorEngbers, Jordan D T
dc.contributor.authorStys, Peter K
dc.contributor.authorZamponi, Gerald W
dc.contributor.authorTurner, Ray W
dc.date.accessioned2018-09-26T12:09:45Z
dc.date.available2018-09-26T12:09:45Z
dc.date.issued2017-08-11
dc.date.updated2018-09-26T12:09:44Z
dc.description.abstractAbstract 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.citationMolecular Brain. 2017 Aug 11;10(1):37
dc.identifier.doihttps://doi.org/10.1186/s13041-017-0317-8
dc.identifier.urihttp://hdl.handle.net/1880/108005
dc.identifier.urihttps://doi.org/10.11575/PRISM/45706
dc.language.rfc3066en
dc.rights.holderThe Author(s).
dc.titleA T-type channel-calmodulin complex triggers αCaMKII activation
dc.typeJournal Article
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