TMEM16C cuts pain no SLACK

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dc.contributor.authorGadotti, Vinícius Maria
dc.contributor.authorZamponi, Gerald W.
dc.date.accessioned2018-05-11T14:06:31Z
dc.date.available2018-05-11T14:06:31Z
dc.date.issued2013-09-01
dc.description.abstractTMEM16C 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.en_US
dc.identifier.citationGadotti, V. M., & Zamponi, G. W. (2013). TMEM16C cuts pain no SLACK. Nature Neuroscience, 16(9), 1165-1166. doi:10.1038/nn.3497en_US
dc.identifier.doihttp://dx.doi.org/10.1038/nn.3497en_US
dc.identifier.urihttp://hdl.handle.net/1880/106631
dc.identifier.urihttps://doi.org/10.11575/PRISM/43816
dc.language.isoenen_US
dc.publisherNature neuroscienceen_US
dc.publisher.departmentPhysiology & Pharmacologyen_US
dc.publisher.facultyCumming School of Medicineen_US
dc.publisher.institutionUniversity of Calgaryen_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0en_US
dc.titleTMEM16C cuts pain no SLACKen_US
dc.typeunknown
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