TMEM16C cuts pain no SLACK

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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Figure 1: Regulation of SLACK channels by TMEM16C.

Katie Vicari

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Correspondence to Gerald W Zamponi.

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The authors declare no competing financial interests.

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Gadotti, V., Zamponi, G. TMEM16C cuts pain no SLACK. Nat Neurosci 16, 1165–1166 (2013). https://doi.org/10.1038/nn.3497

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