Genetic mechanisms of skin differentiation and barrier function in atopic eczema

The development of skin as a functional barrier is essential to maintain human health in the terrestrial environment. Skin barrier dysfunction leads to eczema and other atopic diseases, resulting in a substantial burden of morbidity. Genetic predisposition plays a major role in eczema pathogenesis and a better understanding of molecular mechanisms in atopic skin is required to identify druggable pathways and targets for future drug discovery.
Skin as an organ can be cultured in vitro to produce a model that effectively recapitulates both structural and functional elements of barrier formation and function. Selected genes can be manipulated within the keratinocytes making up this organotypic skin model, using siRNA, viral transfection or CRISPR-cas9 editing, to investigate genetic mechanisms in eczema pathogenesis. Transcriptomic and proteomic analyses allow an unprecedented level of detail in the molecular assessment of these cells and tissues.
The aim of this PhD project is to investigate molecular mechanisms in skin barrier formation, function and dysfunction, to identify genetic risk factors and functional pathways of relevance to atopic eczema. Ultimately we aim to translate this knowledge for the development of more targeted therapy.

Skills and opportunities
This PhD will provide training in primary cell culture, organotypic modelling, skin biology, molecular genetics and proteomic analysis. This translational research offers the opportunity to work on a project with direct clinical relevance.

Applications
To apply please send a curriculum vitae, covering letter explaining why you are interested in this project, and details of three referees to Prof Sara Brown: [Email Address Removed]