TMEM16C cuts pain no SLACK
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Nature neuroscience
Abstract
TMEM16C has an unexpected role in regulating the activity and cell surface expression of sodium-activated potassium (SLACK) channels. By enhancing SLACK currents, TMEM16C indirectly inhibits pain signaling.
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Citation
Gadotti, V. M., & Zamponi, G. W. (2013). TMEM16C cuts pain no SLACK. Nature Neuroscience, 16(9), 1165-1166. doi:10.1038/nn.3497