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A Ca(v)3.2/syntaxin-1A signaling complex controls T-type channel activity and low-threshold exocytosis.
Weiss N., Hameed S., Fernández-Fernández J. M., Fablet K., Karmazinova M., Poillot C., Proft J., Chen L., Bidaud I., Monteil A. et al
Journal of Biological Chemistry 287, 4 (2012) 2810-8 - http://www.hal.inserm.fr/inserm-00757396
A Ca(v)3.2/syntaxin-1A signaling complex controls T-type channel activity and low-threshold exocytosis.
Norbert Weiss1, 2, Shahid Hameed2, José Fernández-Fernández3, Katell Fablet1, Maria Karmazinova4, Cathy Poillot1, Juliane Proft5, Lina Chen2, Isabelle Bidaud6, 7, Arnaud Monteil6, 7, Sylvaine Huc-Brandt6, 7, Lubica Lacinova4, Philippe Lory6, 7, Gerald Zamponi () 2, Michel De Waard () 1
1 :  GIN - U836 - Grenoble Institut des Neurosciences
INSERM : U836 – Université Joseph Fourier - Grenoble I – CHU Grenoble – CEA : DSV/IRTSV
UJF - Site Santé La Tronche - BP 170 - 38042 Grenoble Cedex 9
2 :  Department of Physiology and Pharmacology
Hotchkiss Brain Institute – University of Calgary
T2N4N1 Calgary
3 :  Laboratory of Molecular Physiology and Channelopathies
Universitat Pompeu Fabra
Department of Experimental and Health Science - 08003 Barcelona
4 :  Laboratory of Biophysics
Institute of Molecular Physiology and Genetics – Slovak Academy of Sciences
83334 Bratislava
5 :  Department of Clinical Neurosciences
Hotchkiss Brain Institute – University of Calgary
T2N4N1 Calgary
6 :  Département de Physiologie
Institut de Génomique Fonctionnelle
34094 Montpellier
7 :  IGF - Institut de génomique fonctionnelle
CNRS : UMR5203 – INSERM : U661 – Université Montpellier I – Université Montpellier II - Sciences et techniques
141, Rue de la Cardonille 34094 MONTPELLIER CEDEX 5
INSERM U836, équipe 3, Canaux calciques, fonctions et pathologies
T-type calcium channels represent a key pathway for Ca(2+) entry near the resting membrane potential. Increasing evidence supports a unique role of these channels in fast and low-threshold exocytosis in an action potential-independent manner, but the underlying molecular mechanisms have remained unknown. Here, we report the existence of a syntaxin-1A/Ca(v)3.2 T-type calcium channel signaling complex that relies on molecular determinants that are distinct from the synaptic protein interaction site (synprint) found in synaptic high voltage-activated calcium channels. This interaction potently modulated Ca(v)3.2 channel activity, by reducing channel availability. Other members of the T-type calcium channel family were also regulated by syntaxin-1A, but to a smaller extent. Overexpression of Ca(v)3.2 channels in MPC 9/3L-AH chromaffin cells induced low-threshold secretion that could be prevented by uncoupling the channels from syntaxin-1A. Altogether, our findings provide compelling evidence for the existence of a syntaxin-1A/T-type Ca(2+) channel signaling complex and provide new insights into the molecular mechanism by which these channels control low-threshold exocytosis.
Sciences du Vivant/Neurosciences

Articles dans des revues avec comité de lecture
Journal of Biological Chemistry (J Biol Chem)
Publisher American Society for Biochemistry and Molecular Biology
ISSN 0021-9258 (eISSN : 1083-351X)

calcium channel – T-type – Cav3.2 channel – SNARE – syntaxin-1A – SNAP-25 – exocytosis – neuron – MPC cell
Calcium Channels – T-Type – Cell Line – Exocytosis – Humans – Multiprotein Complexes – Signal Transduction – Syntaxin 1 – Calcium Channels
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