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