A T-type channel-calmodulin complex triggers αCaMKII activation

Ileana Micu, Hadhimulya Asmara, Arsalan P. Rizwan,, Giriraj Sahu, Brett A. Simms,, Fang-Xiong Zhang, Jordan D. T. Engbers, Peter K. Stys, Gerald W. Zamponi, Ray W. Turner

    Research output: Contribution to journalArticle

    11 Citations (Scopus)
    211 Downloads (Pure)

    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.
    Original languageEnglish
    Article number37
    Pages (from-to)1-15
    JournalMolecular Brain
    Volume10
    Issue number1
    DOIs
    Publication statusPublished - 11 Aug 2017

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