Melissa Popowski

Postdoctoral Associate         


A mutation in the Huntingtin protein is the cause of Huntington’s disease, a devastating neurodegenerative disorder. Despite many years of intense scrutiny, the biochemical functions of the wildtype and/or mutant Huntingtin protein remain unclear. Understanding the role of the Huntingtin protein in the cell will give us insight into the role of mutant Huntingtin during disease progression. We aim to discover the role of Huntingtin in pluripotent cells as well as its role during neuronal differentiation and in mature neurons. Previous work in mouse models has shed some light; however they do not completely recapitulate the human disease. We are using human embryonic stem cells in order to discover the function of Huntingtin during these key developmental stages in the hope of developing targeted and effective therapies for Huntington’s disease.

Melissa earned her Bachelors of Science from Southampton College in 2003 in Long Island, NY. Before entering graduate school, she worked at the American Red Cross as a medical technician before beginning graduate school. She earned her Ph.D. from The University of Texas at Austin in 2012. Her dissertation work explored the role of the transcription factor Bright in pluripotency and cellular reprogramming. She joined the Brivanlou lab in the fall of 2013 as a Postdoctoral Associate. Her focus is on discovering the role of the Huntingtin protein in embryonic and neuronal development.