Journal
CHANNELS
Volume 10, Issue 3, Pages 175-184Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/19336950.2016.1138189
Keywords
calcium channel; Ca(v)3; 2; gating; glycosylation; T-type channel
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Funding
- VEGA [2/0044/13]
- Czech Science Foundation [15-13556S]
- Czech Ministry of Education Youth and Sports [7AMB15FR015]
- Institute of Organic Chemistry and Biochemistry (IOCB)
- IOCB
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Low-voltage-gated T-type calcium channels are expressed throughout the nervous system where they play an essential role in shaping neuronal excitability. Defects in T-type channel expression have been linked to various neuronal disorders including neuropathic pain and epilepsy. Currently, little is known about the cellular mechanisms controlling the expression and function of T-type channels. Asparagine-linked glycosylation has recently emerged as an essential signaling pathway by which the cellular environment can control expression of T-type channels. However, the role of N-glycans in the conducting function of T-type channels remains elusive. In the present study, we used human Ca(v)3.2 glycosylation-deficient channels to assess the role of N-glycosylation on the gating of the channel. Patch-clamp recordings of gating currents revealed that N-glycans attached to hCa(v)3.2 channels have a minimal effect on the functioning of the channel voltage-sensor. In contrast, N-glycosylation on specific asparagine residues may have an essential role in the conducting function of the channel by enhancing the channel permeability and / or the pore opening of the channel. Our data suggest that modulation of N-linked glycosylation of hCa(v)3.2 channels may play an important physiological role, and could also support the alteration of T-type currents observed in disease states.
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