Suzanne Zukin
American neuroscientist
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After receiving a bachelor's degree from Bryn Mawr College in 1970, Zukin started her path as a molecular biologist with an understanding of protein structure-function relationships while working on her doctoral dissertation with Donald P. Hollis at Johns Hopkins Medical School. She subsequently pursued postdoctoral work with Daniel E. Koshland Jr. at UC Berkeley where she investigated ligand binding and conformational changes in sensory receptors.
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Neuroscience career and research
In 1977 Suzanne Zukin joined the department of Biochemistry at Albert Einstein College of Medicine.
Currently, the lab is part of the Neuroscience department at Albert Einstein, where Zukin presides as Director of the Neurophsycopharmacology Center and F.M. Kirby Chair in Neural Repair and Protection.
Currently, the lab is pursuing the following research questions related to molecular mechanisms of dysregulation of gene expression of synaptic proteins:
Epigenetic control of synaptic proteins: The Zukin lab researches epigenetic mechanisms that underlie neuronal death in animal models of stroke. They investigate the role of the gene silencing transcription factor RE1-silencing transcription factor (REST) and REST-dependent epigenetic remodeling of genes encoding synaptic proteins. The lab also pursues REST mediated experience-tuning expression of NMDA receptors during development, demonstrating that maternal deprivation disrupts a REST mediated switch to mature NMDA receptor expression
Molecular pathways leading to aberrations in autism and fragile X syndrome: The Zukin lab aims to identify protein expression dysregulation that may result in the phenotypes observed in autism spectrum disorders. The lab has found that the downstream targets of mTORC2, Rho GTPase Rac1 and LIMK exhibit increased expression in a mouse model of autism. Elevated expression of proteins in this pathway are causally related to reduced activity of the actin depolymerizing factor Cofilin, a major determinant of dendritic spine morphology. Another marker of fragile X syndrome that the lab identified is an elevation of GluA2 (GluR2) mRNA as a result of increased CPEB3 protein expression. Elevated GluA2 mRNA increases the percent of AMPA receptors containing GluA2, thus potentially altering the transmission properties and excitation properties of neurons in the brains of individuals with autism spectrum disorders.