About Beth Levine, M.D.
Beth Levine, M.D., was born on April 7, 1960, in Newark, New Jersey. She graduated magna cum laude from Brown University, where she earned a B.A. in French, then attended Cornell University Medical College, earning her M.D. in 1986. Dr. Levine completed her internship and residency in internal medicine at Mount Sinai Hospital in New York and her fellowship in infectious diseases at The Johns Hopkins Hospital.
She began her academic career at Columbia University College of Physicians and Surgeons, where she rose to the rank of associate professor of medicine. In 2004, Dr. Levine was recruited to UT Southwestern as the Jay P. Sanford Professor in Infectious Diseases. She served as Chief of the Division of Infectious Diseases until 2011, when she became the founding Director of UT Southwestern’s Center for Autophagy Research, which Dr. Levine built to include seven faculty members and 23 scientists by 2020.
Dr. Levine was a founding Associate Editor of the journal Autophagy and an editorial board member of Cell and Cell Host & Microbe. She also founded the annual Gordon and Keystone Conferences, devoted to autophagy.
Dr. Levine, a Professor of Internal Medicine and Microbiology and holder of the Charles Sprague Distinguished Chair in Biomedical Science at UT Southwestern, was known for her incisive intellect, demand for scientific rigor, and commitment to mentoring. Her leadership in both clinical medicine and research made her a paragon of the physician-scientist.
Dr. Levine was a Howard Hughes Medical Institute Investigator from 2008 until the time of her death. She was elected to the National Academy of Sciences in 2013.
Dr. Levine's Research
Dr. Levine’s landmark work in autophagy, a pathway of intracellular macromolecule recycling that is conserved throughout eukaryotic organisms, arose from an exploration into the mechanisms by which cells respond to viral infection.
She is known as the founder of the field of mammalian autophagy. In a seminal paper (Nature. 1999;402:672-6), she identified Beclin 1 (BECN1) as a tumor suppressor gene that acted through autophagy, thus moving the field of autophagy (which was previously believed to be limited to yeast) to mammalian biology.
In addition, Dr. Levine demonstrated autophagy’s role in processes from immunity to tumor suppression to aging, thereby establishing its role in mammalian physiology. Her laboratory identified conserved mechanisms underlying the regulation of autophagy (e.g., BCL2-BECN1 complex formation, insulin-like signaling, EGFR, ERBB2/HER2, and AKT1-mediated Beclin 1 phosphosphorylation); and provided the first evidence that autophagy genes are important in antiviral host defense, tumor suppression, life-span extension, apoptotic corpse clearance, metazoan development, Na,K-ATPase-regulated cell death, and the beneficial metabolic effects of exercise.
Dr. Levine’s work filled the void between fundamental cellular biology and human disease. Her focus on biological concepts influenced many scientific disciplines and informed our understanding of dozens of clinical disorders. Her expertise provided the mechanistic insight required to advance the field of autophagy toward targeted therapeutic strategies that apply to a wide range of diseases. Her work was key in forming the basis for several autophagy-inducing therapeutic strategies that are currently under development (e.g., Tat-Beclin 1 peptide and BCL2 disruptor).