Julie Forman-Kay is program head in molecular medicine at the Hospital for Sick Children in Toronto, Canada. She received her B.Sc. in chemistry from the Massachusetts Institute of Technology and her Ph.D. in molecular biophysics andd biochemistry from Yale University. The major focus of her lab is to provide biological insights into how dynamic properties of proteins are related to function and methodological tools to enable better understanding of dynamic and disordered states. Most recently, her lab has probed the biophysics of protein phase separation and how it regulates cellular condensates and biological function.
Julie Forman-Kay
Program head
Hospital for Sick Children
From this contributor
How microscopic ‘condensates’ in cells might contribute to autism
A controversial idea about how cells compartmentalize their contents into droplets — like beads of oil in water — could be key to understanding autism, says Julie Forman-Kay.
How microscopic ‘condensates’ in cells might contribute to autism
Explore more from The Transmitter
New projectome captures ‘complex beast’ of serotonin system in mice
The whole-brain map—the first of its kind in a vertebrate—identifies five distinct neuron groups.
New projectome captures ‘complex beast’ of serotonin system in mice
The whole-brain map—the first of its kind in a vertebrate—identifies five distinct neuron groups.
Silent, motion-resistant fMRI expands scans in behaving mice
The method, called SORDINO, captures brain images in animals while they move and interact.
Silent, motion-resistant fMRI expands scans in behaving mice
The method, called SORDINO, captures brain images in animals while they move and interact.
Autism-linked variants converge on two molecular patterns in mouse brains
Gene activity across 17 autism mouse models occurs in either of two opposing transcriptomic states, supporting the idea that diverse genetic changes may converge on a few recurring biological patterns.
Autism-linked variants converge on two molecular patterns in mouse brains
Gene activity across 17 autism mouse models occurs in either of two opposing transcriptomic states, supporting the idea that diverse genetic changes may converge on a few recurring biological patterns.