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. 2019 May 9;13(1):153–161. doi: 10.1080/19336950.2019.1614415

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© 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — Hypothetical model for altered myogenesis by Ca_v3.2 variants. While the membrane potential of undifferentiated myoblast is about −8 mV, sequential expression of the slow-inactivating voltage-gated ether-a-go-go (EAG) and inward-rectifying Kir2.1 potassium channels brings the membrane potential to approximately −65 mV (red line), allowing window calcium influx through Ca_v3.2 channels (grey line) required for the fusion of myoblasts. Reduced window current caused the by V681L and D1233H mutations results in a decreased window calcium influx (purple line) which potentially compromises early stage myogenesis. Adapted from [30].