User:Chris Glass
Christopher K. Glass, M.D., Ph.D. Professor of Cellular and Molecular Medicine Professor of Medicine School of Medicine University of California, San Diego
Education: 1973-1977 University of California, Berkeley; B.A. Biophysics 1977-1984 University of California, San Diego; M.D., Ph.D. 1984-1985 Internship and Residency in Internal Medicine, Brigham and Women's Hospital Harvard Medical School. 1986-1989 Fellowship in Endocrinology and Metabolism, University of California, San Diego
Faculty Positions (all at UC San Diego): 1989 Assistant Professor of Medicine in Residence, Division of Endocrinology and Metabolism and Division of Cellular and Molecular Medicine 1991 Assistant Professor of Medicine 1995 Associate Professor of Medicine 1999-present Professor of Medicine and Cellular and Molecular Medicine
Selected Honors: 1987-1994, Lucille P. Markey Scholarship for Biomedical Sciences, 1995 Established Investigator, American Heart Association 1995 American Society for Clinical Investigation 2000 Ernst Oppenheimer Award of the Endocrine Society 2006 Association of American Physicians 2008 Honorary Doctorate of Medicine University of Linköping, Sweden 2009 Adjunct Professor, Salk Institute for Biological Sciences
Selected Extramural Service: 1999-2004 Endocrinology Study Section NIH (Chair 2002-2004) 1999-2002 Council, American Society for Clinical Investigation 2001-2002 Co-Chair and Chair Gordon Conference on Hormone Action 2003 Chair, Deuel Conference on Lipids 2003 Co-Chair, 2005, Chair Keystone Conference on PPARs, 2007 Chair, Gordon Conference on Atherosclerosis 2009 Council of the National Institutes of Diabetes, Digestive and Kidney Diseases, NIH, 2010, Co-Chair, Keystone Conference on Atherosclerosis (Joint with Macrophage Biology)
Research Interests: Dr. Glass has had a long-standing interest in elucidating the molecular mechanisms by which sequence specific transcription factors, co-activators and co-repressors regulate the development and function of macrophages. Recent studies have focused on roles of nuclear receptors in inflammation and macrophage biology. His findings include the discovery that the peroxisome proliferator-activated receptor γ (PPARγ) is a negative regulator of macrophage activation, and that macrophage PPARγ exerts crucial anti-inflammatory, anti-atherogenic and anti-diabetic functions in vivo. His laboratory’s recent discovery that PPARγ exerts anti-inflammatory effects in macrophages by preventing the signal-dependent removal of the NCoR corepressor from inflammatory response genes established the concept that NCoR complexes impose a transcription checkpoint that is required to maintain low levels of inflammatory gene expression under basal conditions and function as targets of anti-inflammatory signals. His analysis of genome-wide transcriptional responses to inflammatory stimuli revealed that members of the nuclear receptor superfamily exploit different molecular mechanisms to negatively regulate the expression of cohorts of genes that are linked to distinct biological processes. These findings provided unexpected insights into how signaling pathways that regulate gene expression can be differentially integrated at the level of individual promoters.
