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Altered epidermal lipid processing and calcium distribution in the KID syndrome mouse model Cx26S17F
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 Cx26S...
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| 出版年: | FEBS Lett |
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| 主要な著者: | , , , , , , , , , |
| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
2015
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| 主題: | |
| オンライン･アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4741282/ https://ncbi.nlm.nih.gov/pubmed/26070424 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.febslet.2015.05.047 |
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