Shawn C. Burgess
Dr. Burgess has a strong life sciences background with a particular focus in molecular biology, in vivo drug target validation and genetic engineering. He is currently President and CEO of Atumida, Inc. and co-founder/Chairman of the Board for Medical nanotechnologies, Inc.
He recently held the positions of Vice President of Business Development for the U.K.-based firm Stem Cell Sciences, LLC and Vice President, Research and Development for Zyvex Corporation where he guided a team of 36 scientists and research engineers and played and integral part of the company's restructuring.
Prior to Zyvex, he was empoyed at Serologicals Corporation, a 1000 employee biotools and reagents company realizing $275M in 2005 revenue, as Director of Scientific Sourcing and New Technologies. There he provided long-term visionary guidance for the company regarding new producta nd technology development opportunities through the establishment of key relationships and partnerships with aademic researchers and institutions.
Prior to his appointment there he acted as Senior Director, Functional Genomics and Senior Director, Corporate Business Development for the Serologicals subsisdiary Chemicon International. In these capacities he managed a team of scientists focused on the generation of animal models for human disorders and identified an in-licensed new products and technologies from worldwide industrial and academic sources.
Dr. Burgess' other roles in the biotechnology industry include Co-founder, Board Member and President of Genome BioSciences, Inc. and Founding Scientist for Lexicon Genetics, Inc., where he focused on high-throughput drug target identification and validation at the molecular level. In addition, as NIH-sponsored Research Fellow he conducted research at the University of California San Diego and has published in major scientific journals including Nature and Science on a variety of research in genetic engineering, developmental biology and the molecular control of cellular identity. He also recently published the book "Understanding Nanomedicine: An Introductory Textbook."
1995 BS, Chemistry, The University of Texas at Dallas
1997 MS, Chemistry, The University of Texas at Dallas
2000 Doctorate, Chemistry, The University of Texas at Dallas
2003 Post-doctoral work, UTSW Medical Center
Assistant Professor, Advanced Imaging Center, UTSW Medical Center
Assistant Professor, (Secondary) Dept. of Pharmacology, UTSW Medical Center
Adjunct Assistant Professor, Dept. of Molecular and Cell Biol., The University of Texas at Dallas
Intermediary metabolism is the complex process by which nutrients are transformed into cellular building blocks, redistributed to specific cellular fuels, converted to storage molecules or oxidized to provide energy. Disorders of intermediary metabolism are the basis of many diseases, so techniques that allow quantitative measures of flux of molecules through these metabolic pathways are important tools for basic and clinical science. Nuclear Magnetic Resonance (NMR) spectroscopy in conjunction with stable isotope (non-radioactive) tracers is a powerful technique for understanding intermediary metabolism. NMR is especially informative about the chemical nature of an atom (and its neighboring atoms) in a molecule and thus provides enormous insight into the metabolic fate of isotope labeled tracers. Administration of stable isotope tracers, containing carbon-13 or deuterium, in humans or animals followed by NMR analysis of tissue or fluid extracts reveals the metabolic flux of a number of biochemical pathways. My interest is in using this technology to study hepatic energy production and gluconeogenesis in the liver and kidney. I have studied these pathways with collaborators with mouse models having specific defects in hepatic energy and glucose metabolism and have transitioned the information gained from animal studies towards the understanding of human physiology by partnering with clinicians who have human subjects with abnormal metabolic features such as obesity and diabetes. This powerful cross-disciplinary approach unites my interests in metabolism with molecular biologists and clinicians, providing an increasingly integrated picture of the physiology of metabolic diseases.
1. Burgess SC, Hausler N, Merritt M, Jeffrey FMH, Storey C, Milde A, Koshy S, Lindner J, Magnuson MA, Malloy CR, and Sherry AD. Impaired Tricarboxylic Acid Cycle Activity in Mouse Livers Lacking Cytosolic Phosphoenolpyruvate Carboxykinase. J Biol Chem 279: 48941-48949, 2004.
2. Burgess SC, Jeffrey FMH, Storey C, Milde A, Hausler N, Merritt M, Moulder H, Holm C, Sherry AD, Malloy CR. Effect of Murine Strain on Metabolic Pathways of Glucose Production after Brief or Prolonged Fasting. Am J Physiol Endocrinol Metab 289:E53-61, 2005.
3. Burgess SC, Leone TC, Wende AR, Croce MA, Chen Z, Sherry AD, Malloy CR, and Finck BN. Diminished hepatic gluconeogenesis via defects in tricarboxylic acid cycle flux in peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha)-deficient mice. J Biol Chem 281: 19000-19008, 2006.
4. Browning JD, Davis J, Saboorian MH, and Burgess SC. A low-carbohydrate diet rapidly and dramatically reduces intrahepatic triglyceride content. Hepatology 44: 487-488, 2006. 5. Burgess SC, He T, Yan Z, Lindner J, Sherry AD, Malloy CR, Browning JD, Magnuson MA. Cytosolic Phosphoenolpyruvate Carboxykinase Does Not Solely Control the Rate of Hepatic Gluconeogenesis in the Intact Mouse Liver. Cell Metabolism
5: 313-320, 2007. 6. SC Burgess, T Kitazume, K Iizuka, NH Jeoung, RA Harris, BC. Miller, Y Kashiwaya, RL. Veech and K Uyeda. Mechanisms for the Reduced NAD/NADH REDOX potential and lower energy state of liver of Carbohydrate response element-binding protein (ChREBP) deficient mice. JBC. In PRESS, 2008.
- Updated: February 6, 2006