A T-type channel-calmodulin complex triggers αCaMKII activation

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

doi:10.1186/s13041-017-0317-8

A T-type channel-calmodulin complex triggers αCaMKII activation

Hadhimulya Asmara, Ileana Micu, 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 journal › Article › peer-review

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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 language	English
Article number	37
Pages (from-to)	1-15
Journal	Molecular Brain
Volume	10
Issue number	1
DOIs	https://doi.org/10.1186/s13041-017-0317-8
Publication status	Published - 11 Aug 2017

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10.1186/s13041-017-0317-8Licence: CC BY

A T-type channel-calmodulin complex triggers αCaMKII activation
Copyright 2017 the authors. This is an open access article published under a Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium, provided the author and source are cited.
Final published version, 2.91 MBLicence: CC BY

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@article{ac6736c9a4df4089b535d3cecc9c6354,

title = "A T-type channel-calmodulin complex triggers αCaMKII activation",

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.",

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

year = "2017",

month = aug,

day = "11",

doi = "10.1186/s13041-017-0317-8",

language = "English",

volume = "10",

pages = "1--15",

journal = "Molecular Brain",

issn = "1756-6606",

publisher = "BioMed Central",

number = "1",

}

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

In: Molecular Brain, Vol. 10, No. 1, 37, 11.08.2017, p. 1-15.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - A T-type channel-calmodulin complex triggers αCaMKII activation

AU - Asmara, Hadhimulya

AU - Micu, Ileana

AU - Rizwan,, Arsalan P.

AU - Sahu, Giriraj

AU - Simms,, Brett A.

AU - Zhang, Fang-Xiong

AU - Engbers, Jordan D. T.

AU - Stys, Peter K.

AU - Zamponi, Gerald W.

AU - Turner, Ray W.

PY - 2017/8/11

Y1 - 2017/8/11

N2 - 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.

AB - 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.

U2 - 10.1186/s13041-017-0317-8

DO - 10.1186/s13041-017-0317-8

M3 - Article

VL - 10

SP - 1

EP - 15

JO - Molecular Brain

JF - Molecular Brain

SN - 1756-6606

IS - 1

M1 - 37

ER -

A T-type channel-calmodulin complex triggers αCaMKII activation

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