Felicitas Bosen

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Abrogation of Gap Junctional Communication in ES Cells Results in a Disruption of Primitive Endoderm Formation in Embryoid Bodies

K. Willecke, S. Ergün, A. Pfeifer, 2017, Stem cells.

Disease-linked connexin26 S17F promotes volar skin abnormalities and mild wound healing defects in mice

K. Willecke, D. Laird, Qing Shao, 2017, Cell Death & Disease.

The connexin26 S17F mouse mutant represents a model for the human hereditary keratitis-ichthyosis-deafness syndrome.

K. Willecke, T. Moser, N. Strenzke, 2011, Human molecular genetics.

The Clouston syndrome mutation connexin30 A88V leads to hyperproliferation of sebaceous glands and hearing impairments in mice

K. Willecke, N. Strenzke, T. Franz, 2014, FEBS letters.

From Hyperactive Connexin26 Hemichannels to Impairments in Epidermal Calcium Gradient and Permeability Barrier in the Keratitis-Ichthyosis-Deafness Syndrome.

K. Willecke, A. Pupo, Agustín D. Martínez, 2016, The Journal of investigative dermatology.

Altered epidermal lipid processing and calcium distribution in the KID syndrome mouse model Cx26S17F

K. Willecke, D. Crumrine, P. Dörmann, 2015, FEBS letters.

Disease-linked connexin26 S17F promotes volar skin abnormalities and mild wound healing defects in mice

K. Willecke, D. Laird, Qing Shao, 2017, Cell Death & Disease.

The Connexin40A96S mutation from a patient with atrial fibrillation causes decreased atrial conduction velocities and sustained episodes of induced atrial fibrillation in mice.

K. Willecke, L. Lickfett, J. Schultze, 2013, Journal of molecular and cellular cardiology.

Human Connexin43E42K Mutation From a Sudden Infant Death Victim Leads to Impaired Ventricular Activation and Neonatal Death in Mice

K. Willecke, D. Malan, B. Fleischmann, 2015, Circulation. Cardiovascular genetics.