Gabriel Nuñez, M.D.
Professor of Pathology
Campus Address:
4219 CCGC 0938
1500 East Medical Center Drive
Ann Arbor, Michigan  48109-0938
Telephone:  734/764-8514
Fax:      734/647-9654
Gabriel_Nunez@umich.edu

Annual Report | Biography | Clinical Interests | Research Interests | Selected Publications

Departmental Annual Report

1999-2000

Brief Biography

Dr. Nuñez earned his M.D. degree from the University of Seville Medical School, Seville, Spain, in 1977, and performed an internship at the University Hospital, University of Seville Medical School in Seville. He then served as a Postdoctoral Fellow in Immunology in the Department of Internal Medicine at the University of Texas Health Science Center, Dallas, Texas, from 1979-1982, after which he became a Senior Research Associate in Immunology in the same Department of Internal Medicine. Dr. Nuñez then served as a House Officer in the Department of Pathology at the Washington University School of Medicine, St. Louis, Missouri, from 1985-1990, where he was also a Postdoctoral Fellow, from 1987-1990, in Molecular Biology at the Howard Hughes Medical Institute of the Washington University School of Medicine where he trained in the laboratory of Dr. Stanley Korsmeyer.

In 1991, Dr. Nuñez joined the faculty of the Department of Pathology at the University of Michigan as an Assistant Professor, where he was also the Director of the Molecular Diagnostics Laboratory from 1991-1993. Dr. Nuñez was promoted to Associate Professor of Pathology in 1996. He is co-director of the Cell Biology Program at the University of Michigan Cancer Center.

Dr. Nuñez's clinical interests deal with molecular diagnostics, while his research interests are directed towards understanding the molecular and cellular regulation of programmed cell death (PCD) or apoptosis.

Dr. Nuñez was promoted to Professor in 2001.

Clinical Interests

Pathology, Molecular diagnostics

Research Interests

Molecular biology, Apoptosis

Dr. Nuñez's laboratory is interested in signaling pathways leading to apoptosis and NF-kappaB activation. In particular, the laboratory is focused on the characterization of signaling molecules that regulate caspases, a family of cysteine proteases that execute the cell death program. These include Bcl-2 family members, a conserved family of molecules that regulate apoptosis and caspase activation. Another class include Apaf-1, a major activator of caspase-9. Several Apaf-1-like molecules including Nod1 and Nod2 have been identified in our laboratory and are being characterized. Nods are intracellular proteins that appear to regulate the host response to pathogens. Recent work in our laboratory indicates that Nod2 is a susceptibility gene for Crohn's disease, a chronic inflammatory disorder of the gastrointestinal tract. Studies in our laboratory are aimed at understanding the role of Nods in innate immunity and the mechanism by which genetic alteration in Nod2 promotes Crohn's disease. Finally, our laboratory has identified CIPER/Bcl10, a protein involved in the development of a subset of MALT lymphomas in humans. Bcl10 activates NF-kappaB and promotes lymphoid survival. Studies to characterize the Bcl10 signaling pathway are in progress.

Selected Publications

Hu Y, Benedict MA, Ding L, Nuñez G. Role of cytochrome c and dATP/ATP hydrolysis in Apaf-1-mediated caspase-9 activation and apoptosis. EMBO J. 18(13):3586-3595 (1999).
Inohara N, Koseki T, Lin J, del Peso L, Lucas PC, Chen FF, Ogura Y, Nuñez G: An induced proximity model for NF-kappa B activation in the Nod1/RICK and RIP signaling pathways. J Biol Chem. 275:27823-31 (2000).