Expression of KID syndromic mutation Cx26S17F produces hyperactive hemichannels in supporting cells of the organ of Corti

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Date

2023-01-09

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journal article

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Investigación
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Authors

Abbott, Ana C., Garcia, Isaac E., Villanelo, Felipe, Flores-Muñoz, Carolina, Ceriani, Ricardo, Maripillán, Jaime, Novoa-Molina, Joel, Figueroa-Cares, Cindel, Perez-Acle, Tomas, Sáez, Juan C., Sanchez, Helmuth A., Martinez, Agustin D.

Publisher

FRONTIERS MEDIA SA

URI

https://repositorio.udla.cl/handle/udla/1406

DOI

https://doi.org/10.3389/fcell.2022.1071202

Keywords

connexin, hemichannel, gap junction, syndromic deafness, cochlea, organ of Corti

Citation

Frontiers in Cell and Developmental Biology, 10, 1071202. https://doi.org/10.3389/fcell.2022.1071202

Abstract

Some mutations in gap junction protein Connexin 26 (Cx26) lead to syndromic deafness, where hearing impairment is associated with skin disease, like in Keratitis Ichthyosis Deafness (KID) syndrome. Th...

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Creative Commons Attribution 4.0 International
Except where otherwised noted, this item's license is described as Creative Commons Attribution 4.0 International
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