Journal
SCIENTIFIC REPORTS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-017-11591-5
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Funding
- Czech Science Foundation [15-13556S]
- Czech Ministry of Education Youth and Sports [7AMB15FR015]
- Institute of Organic Chemistry and Biochemistry (IOCB)
- IOCB
- Canadian Institutes of Health Research (CIHR)
- Alberta Innovates-Health Solutions
- CIHR [10677]
- Canada Research Chair in Biotechnology and Genomics-Neurobiology
- CURE - Taking Flight Award
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Low-voltage-activated T-type calcium channels are essential contributors to the functioning of thalamocortical neurons by supporting burst-firing mode of action potentials. Enhanced T-type calcium conductance has been reported in the Genetic Absence Epilepsy Rat from Strasbourg (GAERS) and proposed to be causally related to the overall development of absence seizure activity. Here, we show that calnexin, an endoplasmic reticulum integral membrane protein, interacts with the III-IV linker region of the Ca(v)3.2 channel to modulate the sorting of the channel to the cell surface. We demonstrate that the GAERS missense mutation located in the Ca(v)3.2 III-IV linker alters the Ca(v)3.2/calnexin interaction, resulting in an increased surface expression of the channel and a concomitant elevation in calcium influx. Our study reveals a novel mechanism that controls the expression of T-type channels, and provides a molecular explanation for the enhancement of T-type calcium conductance in GAERS.
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