A Legacy of Research & Discovery
Nobel Prizes
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UT Southwestern Nobel Prize Recipients:
Michael S. Brown, M.D., & Joseph L. Goldstein, M.D. // 1985
Cholesterol Regulation
Drs. Brown and Goldstein shared the Nobel Prize in Physiology or Medicine in 1985 for their discoveries of how the body regulates cholesterol and the treatment of diseases caused by abnormally elevated cholesterol levels in the blood. They found that human cells have low-density lipoprotein (LDL) receptors that remove cholesterol from the blood and that when LDL receptors are not present in sufficient numbers, individuals become at risk for cholesterol-related diseases. It was a pioneering discovery that would lead to the development of statins, which help regulate cholesterol, improve the quality of life for millions of people, and save lives.
Johann Deisenhofer, Ph.D. // 1988
Membrane Protein Structure
Dr. Deisenhofer shared the Nobel Prize in Chemistry in 1988 for his use of X-ray crystallography to describe the structure of a protein involved in photosynthesis. One of the most fundamental processes of life is photosynthesis, which uses energy from sunlight to make sugars out of water and carbon dioxide, providing nourishment for plant life to exist. Studying bacteria, researchers discovered how energy is converted through a series of proteins that transport electrons and were then able to create a model and determine the three-dimensional structure for the photosynthetic reaction center. Their work provided unique insight into photosynthesis, helping scientists understand how energy is transferred into biological systems.
Alfred G. Gilman, M.D., Ph.D. // 1994
Cell Signaling
Dr. Gilman shared the Nobel Prize in Physiology or Medicine in 1994 for discovery of G-proteins and the role they play in the complex processes by which cells communicate with each other. Dr. Gilman, who died in 2015, determined that certain leukemia cells lacked the G-protein and discovered a way to restore the cell’s function by using G-proteins from other cells, such as those in the brain. The missing protein was given the name G-protein because it reacts with GTP, one of the building blocks needed for the synthesis of RNA during the transcription process, to modulate signals in cells. Disruptions in signal modulation can lead to disease and tumors and have been documented not only in leukemia, but in other diseases such as cholera, diabetes, and alcoholism. Dr. Gilman contributed groundbreaking research that has helped researchers around the world to further the understanding of the roles G-proteins play in human disease.
Bruce A. Beutler, M.D. // 2011
Innate Immunity
Dr. Beutler shared the Nobel Prize in Physiology or Medicine in 2011 for his discovery of how the immune system is activated. When bacteria, viruses, and other microorganisms attack the body, receptor proteins recognize such microorganisms and activate innate immunity, the first step in the body’s immune response. Through a series of experiments, Dr. Beutler revealed how cells detect infection and how the innate immune system is activated in response to infection. His work helped open new avenues for the development of therapies against infections, cancer, and inflammatory diseases.
Thomas C. Südhof, M.D. // 2013
Synapses and Neural Function
Dr. Südhof shared the Nobel Prize in Physiology or Medicine in 2013 for his discovery of the machinery regulating tiny packets of information that are exchanged between nerve cells. Cells produce and export many molecules, which are transported through the cell in small packages called vesicles. Researchers discovered molecular principles that govern how this cargo is delivered in the cell to the right place at the right time. Dr. Südhof, former Chair of the Department of Neuroscience at UT Southwestern who is now at Stanford University School of Medicine, revealed how signals instruct vesicles to release their cargo with precision. Disturbances in this system have deleterious effects and contribute to conditions such as neurological diseases, diabetes, and immunological disorders.