
Christopher Glass
Affiliation: UCSD SOM
Professor of Medicine
cglass@ucsd.edu
Phone: 858-534-6011
Biography
Dr. Glass received his Bachelors degree in Biophysics from the University of California, Berkeley and his M.D. and Ph.D. degrees from the University of California, San Diego. Following internship and residency training in Internal Medicine at Harvard Medical School’s Brigham and Women’s Hospital, Dr. Glass returned to UCSD for clinical and research fellowships in Endocrinology and Metabolism. His post doctoral studies with Dr. Michael G. Rosenfeld focused on regulation of growth hormone gene expression by thyroid hormone and retinoic acid receptors. Dr. Glass’ laboratory currently investigates roles of nuclear receptors and other signal-dependent transcription factors in the regulation of macrophage development and function. Dr. Glass holds joint appoints in the Department of Cellular and Molecular Medicine and the Department of Medicine.
Research Summary
Dr. Glass' laboratory investigates the mechanisms by which sequence-specific transcription
factors regulate the development and function of macrophages. A major focus is on
members of the nuclear receptor, AP-1 and Ets families of transcription factors. These
factors bind to regulatory regions in target genes and act as positive or negative regulators
of gene expression. Nuclear receptors regulate gene expression in response to the binding
of small molecular weight ligands that diffuse into cells, while AP-1 and Ets factors are
regulated by phosphorylation. Studies over the past few years have led to the identification
of a large number of coactivator and corepressor complexes that interact with these factors
in a ligand or signal-dependent manner and mediate their transcriptional effects. Several of
these complexes are illustrated in the accompanying figure. Current efforts are to
determine the biochemical and biological roles of these transcription factors and their
associated co-regulators in controlling macrophage differentiation and function. A
combination of biochemical, cellular and in vivo model systems are used, incorporating
macrophage-specific knockouts, microarray technologies and bioinformatics approaches to
unravel the contributions of specific factors to the development of specialized macrophage
functions and the pathogenesis of atherosclerosis and inflammatory diseases. Specific
ongoing projects in the laboratory include:
Studies of the mechanisms by which Ets transcriptional repressors inhibit macrophage
proliferation
Studies of the mechanisms by which members of the nuclear receptor family regulate the
evolution of inflammatory responses
Studies of the mechanisms by which nuclear hormone receptors regulate cholesterol and
fatty acid homeostasis in macrophages
Studies of how co-activators and co-repressors serve as signaling integrators during
inflammatory responses
Trainees have opportunities to participate in all aspects of these studies.

References
References From PubMed (NCBI)