Hoon Ryu, PhD
|Institution||Boston University School of Medicine|
|Address||150 S Huntington Avenue|
Jamaica Plain MA 02130
|Institution||VA Boston Healthcare System|
Dr. Hoon Ryu earned his doctoral degree from Chonbuk National University, South Korea. He completed a postdoctoral research fellowship and was appointed Instructor of Neurology at Beth Israel Deaconess Medical Center and Harvard Medical School in 1999. He joined the Boston University School of Medicine’s Department of Neurology in 2004 as an Assistant Professor. Now he is an Associate Professor and an investigator with the Boston University Alzheimer’s Disease Center and VA Boston Healthcare System. He is a director of the laboratory for Neuronal Gene Regulation and Epigenetics. He works on the identification of biomarkers, the determination of molecular genetic, epigenetic mechanisms, and the development of therapeutics using cell culture systems and animal models of neurodegeneration. He has published over 70 original reports.
Epigenetic changes encompass an array of molecular modifications including DNA methylation and changes to the chromatin packaging of DNA by post-translational histone modifications. The structure, dynamics, and chemical properties of chromatin almost completely determines how, when, and which genes are turned on and off. Chromatin remodeling and transcription regulation are tightly controlled under physiological conditions. Deregulation of chromatin remodeling is linked to the pathogenesis of neurodegenerative disorders but the mechanism is elusive. In order to identify how genomes are deregulated by heterochromatin, Dr. Ryu is performing ChIP genome-wide sequencing combined with RNA-sequencing followed by platform integration analysis. He has found that altered chromatin plasticity is closely linked to the pathogenesis of Huntington’s disease via an expression of ESET (ERG-associated protein with a SET domain), a histone H3K9-specific methyltransferase. Currently, he is conducting research about mechanisms of ESET gene induction and neuronal heterochromatin condensation in Alzheimer’s disease.
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