My research in graduate school was studying the regulation of the human myelin gene PLP1 which encodes the most abundant protein present in myelin from the central nervous system. Its expression in oligodendrocytes is tightly regulated and disruption of this gene in humans may result in Pelizaeus-Merzbacher disease (PMD) or spastic paraplegia type 2 (SPG2). Primary progressive multiple sclerosis (MS) is also a phenotype of a point mutation in PLP1. I showed where, when, and how that gene is expressed and that the enhancer wmN1 appears to be central to the regulation of PLP1. Combining a novel gene therapy and an existing medication might lead us to a therapy that could reverse some diseases.

In my postdoctoral research I continued working in neuroscience. I worked on the cellular and molecular mechanisms that control the formation and maintenance of Axon Initial Segment and the nodes of Ranvier in both the peripheral and central nervous systems. Using the tool BioID I helped to identify many neuronal proteins which include extracellular matrix molecules, cell adhesion molecules that promote neuron-glia interaction, and cytoskeletal proteins that stabilize the membrane protein complex. I always try to learn and develop new techniques and methods.