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Michael Washburn

Michael Washburn

Talk title: Integrated Analyses of Epigenetic Complexes and Networks

Biography:

Michael Washburn graduated with a B.A. in Chemistry from Grinnell College in 1992 and a PhD in Biochemistry/Environmental Toxicology from Michigan State University in 1998 under the direction of Dr. William W. Wells in the Department of Biochemistry. In 1999, he joined the lab of Dr. John R. Yates, III at the University of Washington as a post-doctoral scientist. When Dr. Yates relocated his lab to the Scripps Research Institute in San Diego in 2000, Mike continued to work with Dr. Yates as a staff scientist at the Torrey Mesa Research Institute, which was part of Novartis and then Syngenta prior to closing. In 2003, Mike joined the Stowers Institute for Medical Research in Kansas City, MO as the Director of Proteomics. He is also an affiliated Professor in the Department of Pathology and Laboratory Medicine at the University of Kansas Medical Center.

Abstract: Integrated Analyses of Epigenetic Complexes and Networks

Michael P. Washburn, PhD
Stowers Institute for Medical Research
Kansas City, MO USA

Chromatin remodeling proteins, complexes, and networks paly critical roles in human biology and diseases. We integrate multiple technologies to study these systems. To begin, proteins of interest are affinity purified using the multi-functional HaloTag, which allows us to make one cell type and conduct multiple experiments. Using MudPIT and the dNSAF label free quantitative proteomics approach, we determine protein complex content and protein interaction networks, which we visualize using advanced computational tools like topological data analysis. We then employ state of the art microscopy techniques to analyze proteins of interest to analyze interactions in live cells. To gain deeper insight into these complexes and networks we will often perturb the systems using gene deletions, truncations, mutations, or drug treatments, for example. A major focus of the group is currently on the human Sin3 histone deacetylase (HDAC) containing complexes and their perturbation by the anticancer drug Vorinostat.