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Article

Aberrant connexin26 hemichannels underlying keratitis-ichthyosis-deafness syndrome are potently inhibited by mefloquine.

The Journal of investigative dermatology - 1 Apr 2015

Levit Noah A, Sellitto Caterina, Wang Hong-Zhan, Li Leping, Srinivas Miduturu, Brink Peter R, White Thomas W

Abstract excerpt

Keratitis-ichthyosis-deafness (KID) syndrome is an ectodermal dysplasia caused by dominant mutations of connexin26 (Cx26). Loss of Cx26 function causes nonsyndromic sensorineural deafness, without consequence in the epidermis. Functional analyses have revealed that a majority of KID-causing mutations confer a novel expansion of hemichannel activity, mediated by connexin channels in a nonjunctional configuration....

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Identifiers

PMID: 25229253
DOI: 10.1038/jid.2014.408
PMCID: PMC4363291

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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Aberrant connexin26 hemichannels underlying keratitis-ichthyosis-deafness syndrome are potently inhibited by mefloquine.PMID 25229253Read ↗

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