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Article

Altered CO2 sensitivity of connexin26 mutant hemichannels in vitro.

Physiological reports - 1 Nov 2016

de Wolf Elizabeth, van de Wiel Joseph, Cook Jonathan, Dale Nicholas

Abstract excerpt

Connexin26 (Cx26) mutations underlie human pathologies ranging from hearing loss to keratitis ichthyosis deafness (KID) syndrome. Cx26 hemichannels are directly gated by CO2 and contribute to the chemosensory regulation of breathing. The KID syndrome mutation A88V is insensitive to CO2, and has a dominant negative action on the CO2 sensitivity of Cx26WT hemichannels, and reduces respiratory drive in humans. We...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Identifiers

PMID: 27884957
DOI: 10.14814/phy2.13038
PMCID: PMC5357999

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Altered CO2 sensitivity of connexin26 mutant hemichannels in vitro.PMID 27884957Read ↗

Connexin26 hemichannels with a mutation that causes KID syndrome in humans lack sensitivity to CO2.Semantic proximity Read ↗

Opposing modulation of Cx26 gap junctions and hemichannels by CO <sub>2</sub>Semantic proximity Read ↗

Pathological hemichannels associated with human Cx26 mutations causing Keratitis-Ichthyosis-Deafness syndrome.Semantic proximity Read ↗

Chimeric evidence for a role of the connexin cytoplasmic loop in gap junction channel gating.Semantic proximity Read ↗

The human Cx26-D50A and Cx26-A88V mutations causing keratitis-ichthyosis-deafness syndrome display increased hemichannel activity.Semantic proximity Read ↗

Structures of wild-type and a constitutively closed mutant of connexin26 shed light on channel regulation by CO2.Semantic proximity Read ↗

Analysis of trafficking, stability and function of human connexin 26 gap junction channels with deafness-causing mutations in the fourth transmembrane helix.Semantic proximity Read ↗

Keratitis-ichthyosis-deafness syndrome-associated Cx26 mutants produce nonfunctional gap junctions but hyperactive hemichannels when co-expressed with wild type Cx43.Semantic proximity Read ↗

Three-dimensional structure of a human connexin26 gap junction channel reveals a plug in the vestibule.Semantic proximity Read ↗

Connexin mutations causing skin disease and deafness increase hemichannel activity and cell death when expressed in Xenopus oocytes.Semantic proximity Read ↗

Connexin 26 (GJB2) mutations, causing KID Syndrome, are associated with cell death due to calcium gating deregulation.Semantic proximity Read ↗

Dominant connexin26 mutants associated with human hearing loss have trans-dominant effects on connexin30.Semantic proximity Read ↗

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