A postdoctoral position is available to investigate the pathobiology of Sturge-Weber Syndrome (SWS), a rare vascular disorder characterized by vascular lesions involving dermal facial capillaries, the leptomeninges, and vessels in the eye. Our collaborative group determined that the cause of SWS is a somatic, mosaic, activating mutation in the GNAQ gene, encoding the G protein subunit alpha q (see PMID: 23656586). We have now generated an engineered mouse strain that expresses the wild-type GNAQ transcript, but upon Cre recombination, switches to express the mutant transcript. The goal of this project is to utilize this mouse to generate a robust mouse model of the disease, and using this tool, investigate the molecular mechanisms of vascular
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