ArticleFEBS letters2015
Altered epidermal lipid processing and calcium distribution in the KID syndrome mouse model Cx26S17F.
Article in FEBS letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Calcium Regulation of Connexin Hemichannels.International journal of molecular sciences · 2024Review
- Connexin hemichannel inhibition ameliorates epidermal pathology in a mouse model of keratitis ichthyosis deafness syndrome.Scientific reports · 2021Article
- Review
- A potent antagonist antibody targeting connexin hemichannels alleviates Clouston syndrome symptoms in mutant mice.EBioMedicine · 2020Article
- Allele-Specific Small Interfering RNA Corrects Aberrant Cellular Phenotype in Keratitis-Ichthyosis-Deafness Syndrome Keratinocytes.The Journal of investigative dermatology · 2020Article
- Molecular Mechanism of Epidermal Barrier Dysfunction as Primary Abnormalities.International journal of molecular sciences · 2020Review
- Patients with congenital ichthyosis and TGM1 mutations overexpress other ARCI genes in the skin: Part of a barrier repair response?Experimental dermatology · 2019Article
- Connexins and Disease.Cold Spring Harbor perspectives in biology · 2018Review
- Disruption of the lens circulation causes calcium accumulation and precipitates in connexin mutant mice.American journal of physiology. Cell physiology · 2018Article
- Human diseases associated with connexin mutations.Biochimica et biophysica acta. Biomembranes · 2018Review
- Induction of cell death and gain-of-function properties of connexin26 mutants predict severity of skin disorders and hearing loss.The Journal of biological chemistry · 2017Article
- Disease-linked connexin26 S17F promotes volar skin abnormalities and mild wound healing defects in mice.Cell death & disease · 2017Article
- Design and Characterization of a Human Monoclonal Antibody that Modulates Mutant Connexin 26 Hemichannels Implicated in Deafness and Skin Disorders.Frontiers in molecular neuroscience · 2017Article
- Connexinopathies: a structural and functional glimpse.BMC cell biology · 2016Review
- Connexin channels in congenital skin disorders.Seminars in cell & developmental biology · 2016Review
- The role of epidermal sphingolipids in dermatologic diseases.Lipids in health and disease · 2016Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The keratitis-ichthyosis-deafness (KID) syndrome is caused by mutations in the gap junctional channel protein connexin 26 (Cx26), among them the mutation Cx26S17F. Heterozygous Cx26S17F mice resemble the human KID syndrome, i.e. exhibiting epidermal hyperplasia and hearing impairments. Newborn Cx26S17F mice show a defective epidermal water barrier as well as altered epidermal lipid secretion and location. Linoleoyl ω-esterified ceramides are strongly decreased on the skin surface of Cx26S17F mice. Moreover, the epidermal calcium gradient is altered in the mutant mice. These alterations may be caused by an abnormal Cx26S17F channel function that leads to a defective epidermal water barrier, which in turn may trigger the hyperproliferation seen in the KID syndrome.
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Registered trials
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