期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 287, 期 4, 页码 2810-2818出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M111.290882
关键词
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资金
- Alberta Innovates, Health Solutions (AIHS)
- Hotchkiss Brain Institute
- Spanish Ministry of Science and Innovation
- Fondos Europeos de Desarrollo Regional (FEDER) Funds, and Plan E [SAF2009-13182-C03-02]
- Fondo de Investigacion Sanitaria [Red HERACLES RD06/0009]
- Generalitat de Catalunya [2009SGR1369]
- VEGA [2/0195/10]
- Canadian Institutes of Health Research
- [ANR-2006-Neuro35]
- [ANR-09-MNPS-035]
T-type calcium channels represent a key pathway for Ca2+ 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 Ca2+ channel signaling complex and provide new insights into the molecular mechanism by which these channels control low-threshold exocytosis.
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