Altered epidermal lipid processing and calcium distribution in the KID syndrome mouse model Cx26S17F
作者:, Klaus Willecke
摘要: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.
关键词:
论文方向:[{"id":13,"name":"细胞生物学"},{"id":879,"name":"生物化学"}]
发表期刊:FEBS Letters Volume 589, Issue 15
发表时间:Wed Jul 08 00:00:00 CST 2015
数字识别码:10.1016/j.febslet.2015.05.047
是否作者本人: 否
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