about the PI
Stephen Fancy, PhD, DVM
Steve trained in Veterinary Medicine at the University of Cambridge in the United Kingdom, achieving his BA in 1999 and Doctor of Veterinary Medicine in 2002. He went on to join the lab of Professor Robin Franklin at Cambridge University, a leading expert in the mechanisms of white matter injury repair in human multiple sclerosis (MS), to undertake his PhD. He became particularly interested in the transcription factors that control oligodendrocyte maturation, and why the remyelination repair process fails in certain MS patients, identifying a crucial role for the bHLH transcription factor Olig1 in promoting the differentiation of oligodendrocytes in repair of mammalian CNS.
He joined the lab of Professor David Rowitch at the University of California at San Francisco (UCSF) in 2007 to undertake a post-doc. It was clear that there were many factors involved in the myelin repair response and oligodendrocyte maturation that were yet to be discovered. In order to elucidate novel fundamental mechanisms in oligodendrocyte biology, he employed a genome-wide in situ hybridization screen to identify transcription factors expressed in mouse models of remyelinating CNS lesions. From this he identified the wnt pathway as a critical inhibitory pathway for oligodendrocyte maturation, controlling the timing of this process, and that wnt dysregulation could lead to a failed myelin repair response.
He joined the departments of Pediatrics and Neurology and the Newborn Brain Research Institute at UCSF as an Assistant Professor in Residence in 2013, and is currently an Associate Professor in residence. He has a laboratory in the Sandler Neurosciences building at Mission Bay UCSF. The lab remains interested in key questions surrounding oligodendrocyte biology and functions in development and disease, recently identifying how oligodendrocyte precursors migrate around the developing nervous system, using vasculature as a physical scaffold for motility. The lab remains dedicated to and passionate about achieving a better understanding of why myelin repair fails in human demyelinating injuries and continues to elucidate fundamental mechanisms in oligodendrocyte biology.