Figure S5.
Hemicentin-1 deficiency effect on KIF organization in primary keratinocytes. Primary keratinocytes cells grown to 60% confluence on glass coverslips in 12 wells plates were downregulated for hemicentin 1 with a specific siRNA (siHMCN1) or with a control siRNA (siControl), and co-transfected with an empty vector (EV) or expression vectors encoding either WT cDNA or mutant (Mut) KRT14 cDNA carrying the c.373C>T, p.Arg125Cys variant for 48 h at 37°C. The cells were stained for KRT14 expression (red staining) and DAPI (blue staining). The experiment was repeated twice. Cells were visualized by confocal microscopy. Note decreased K14 expression upon HMCN1 silencing and protein aggregates in cells transfected with the mutant KRT14, with marked aggravation in siHMCN1-transfected cells (scale bar = 10 μm).

Hemicentin-1 deficiency effect on KIF organization in primary keratinocytes. Primary keratinocytes cells grown to 60% confluence on glass coverslips in 12 wells plates were downregulated for hemicentin 1 with a specific siRNA (siHMCN1) or with a control siRNA (siControl), and co-transfected with an empty vector (EV) or expression vectors encoding either WT cDNA or mutant (Mut) KRT14 cDNA carrying the c.373C>T, p.Arg125Cys variant for 48 h at 37°C. The cells were stained for KRT14 expression (red staining) and DAPI (blue staining). The experiment was repeated twice. Cells were visualized by confocal microscopy. Note decreased K14 expression upon HMCN1 silencing and protein aggregates in cells transfected with the mutant KRT14, with marked aggravation in siHMCN1-transfected cells (scale bar = 10 μm).

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