David D. Moore is a molecular biologist whose work has focused on the diverse functions of the members of the nuclear hormone receptor superfamily. His contributions stretch from the initial discovery of several family members through the unraveling of their basic functions to a deeper understanding of their roles in both health and disease. Moore was born in Boston, Massachusetts and grew up in Cincinnati, Ohio. His undergraduate degree from Brown University in 1974 was in Molecular Biology, as was his 1979 Ph.D. from the University of Wisconsin-Madison. After a two year postdoctoral fellowship in biochemistry at the University of California-San Francisco, he was a founding faculty member in the new Department of Molecular Biology at Massachusetts General Hospital. He was also in the Genetics Department at Harvard Medical School. In 1997 he moved to the Department of Molecular and Cellular Biology at Baylor College of Medicine in Houston. He has been an active member of the Endocrine Society for many years and is a member of the National Academy of Sciences.

Research Interests

David Moore has made seminal discoveries in the roles of nuclear hormone receptors in health and disease. The 48 family members of this superfamily include the steroid receptors and a larger number of proteins termed orphan receptors whose functions and cognate hormones were initially not known. The Moore laboratory's efforts in this field started with the discovery of several orphan family members, including CAR and SHP. He has also contributed to the identification of new ligands and signaling mechanisms, including the discovery of a new class of ligands termed inverse agonists that do not depend on agonist displacement for their inhibitory effects on agonist-independent receptors. More recently, he has focused on the physiologic functions and disease relevance of several orphans and former orphans that act in the liver, including CAR and the bile acid receptor FXR. Following the leads that these and other receptors have provided, he has driven our current understanding of them as key metabolic regulators that maintain healthy homeostasis when they function appropriately, but can drive pathologic responses when dysregulated.

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Section 42: Medical Physiology and Metabolism