Our Science – Meier Website
Jordan L. Meier, Ph.D.
Dr. Meier received his undergraduate degree in chemistry from Creighton University in 2004, getting introduced to research as an National Science Foundation REU student. Following graduation he moved to the University of California-San Diego, performing graduate research in natural products biochemistry and proteomics under the mentorship of Professor Michael D. Burkart. After receiving his Ph.D. in chemistry in 2009, he moved to the California Institute of Technology. His research as an American Cancer Society postdoctoral fellow in the laboratory of Professor Peter B. Dervan focused on the development of high-throughput sequencing methods to analyze small molecule-DNA interactions.
In 2013, Dr. Meier joined the NCI, where his research focuses on the development of synthetic probes to investigate metabolic and epigenetic signaling pathways in cancer.
Cofactor-Based Profiling of Chromatin Modifiers
Enzyme cofactors link cellular metabolism with the regulation of genome function through the activity of chromatin-modifying enzymes. A major focus of the laboratory is to integrate cofactor-based synthetic probes with high-throughput approaches for the proteomic, genomic, and structural characterization of chromatin modifiers. The goal of these studies is to expand the pharmacological map of epigenomic regulators involved in cancer, and to generate new knowledge for structure-based design, screening, and inhibitor development efforts.
Metabolic Regulation of Epigenetic Signaling
Recent studies have shown that many enzymes active in epigenetic mechanisms of genomic regulation are sensitive to the metabolic state of the cell. A second major aim of the lab is to understand the mechanisms by which metabolic perturbations influence genomic signaling mediated by chromatin modifying enzymes. Long term goals of this work include: 1) the discovery of biological mechanisms underlying oncometabolite-driven cancers, 2) the development of new diagnostics for cancers driven by metabolic mutations, and 3) the identification of small molecules which inhibit epigenetic modifications through metabolic disruption.
This page was last updated on 5/2/2014.