David Ginsburg is James V. Neel Distinguished University Professor of Internal Medicine, Human Genetics and Pediatrics, Warner-Lambert/Parke-Davis Professor of Medicine, a member of the Life Sciences Institute at the University of Michigan Medical School, and a Howard Hughes Medical Institute Investigator. He received his BA from Yale University in 1974 and his MD from Duke University in 1978. Dr. Ginsburg is board certified in Internal Medicine, Hematology, Oncology, and Clinical Genetics. His postdoctoral clinical and research training was at the Brigham and Women’s Hospital and Children’s Hospital, Harvard Medical School. Dr. Ginsburg joined the University of Michigan faculty as an Assistant Professor in 1985. He is a member of the NAS, NAM, American Academy of Arts and Sciences, and the American Philosophical Society. He is recipient of the E. Donnall Thomas Prize and Stratton Medal from the American Society of Hematology, the Basic Research Prize and the Distinguished Scientist Award from the American Heart Association, the Stanley J. Korsmeyer Award from the American Society of Clinical Investigation, and the AAMC Award for Distinguished Research in the Biomedical Sciences. Dr. Ginsburg has served on the Councils for the AAP, the National Academy of Sciences, and the National Academy of Medicine.

Research Interests

Dr. Ginsburg's laboratory studies the components of the blood-clotting system and how disturbances in their function lead to human bleeding and blood-clotting disorders. The lab has studied the molecular basis of the common disorder von Willebrand disease and is identifying modifier genes that control severity for this and related diseases. The lab has also defined mutations in ADAMTS13, an enzyme that processes von Willebrand factor, as the cause of Thrombotic Thrombocytopenia Purpura. The lab also studies the plasminogen activation system, the mechanism by which blood clots are broken down, and has explored the role of this system in a variety of disease processes including atherosclerosis and microbial infection. Finally, studies of the bleeding disease combined deficiency of factors V and VIII identified mutations in a novel pathway for the transport of a select subset of proteins from the ER to the Golgi, leading the Ginsburg lab to further exploration of the intracellular secretory machinery and its role in human disease.

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Primary Section

Section 41: Medical Genetics, Hematology, and Oncology

Secondary Section

Section 42: Medical Physiology and Metabolism