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Contact

 

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)

 

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©2008 UCSD/Burnham Molecular Pathology Graduate Program