Greg Lemke

Biosketch

Greg Lemke, PhD is Françoise Gilot-Salk Distinguished Professor Emeritus and former Chief Science Officer at the Salk Institute for Biological Studies. He received his SB in Life Sciences from the Massachusetts Institute of Technology in 1978 and his PhD in Biology from the California Institute of Technology in 1983. He was a postdoctoral fellow in molecular biology at Columbia University College of Physicians and Surgeons until 1985, when he joined the faculty of the Salk Institute as a member of the Molecular Neurobiology Laboratory. He was also Adjunct Professor in the Department of Neurosciences at UC San Diego from 1995-2024. He is a Fellow of the American Association for the Advancement of Science. He has served on science advisory boards at the Hereditary Disease Foundation, the Helmholtz Gemeinschaft, the Lupus Research Foundation, the University of Basel, the Pew Charitable Trusts, and the Florey Institute. Awards include a Pew Scholars Award, a Rita Allen Scholars Award, and a Javits Neuroscience Investigator Award from the NIH.

Research Interests

Dr. Lemke's research has centered on deciphering the role that receptor tyrosine kinases (RTKs) play in embryonic development, adult physiology, and disease. He discovered 11 of the 58 RTKs encoded in mammalian genomes, defined the TAM and DDR RTK families, and identified new members of the ErbB, FGF, and Eph families. His generation of mouse mutants for ErbB4 and purification of the ErbB ligand neuregulin-1 revealed essential roles for ErbB signaling in Schwann cell development and cardiac morphogenesis. His genetic perturbation of EphA receptor gradients in the retina provided the definitive demonstration that these gradients specify topographic wiring of neuronal connections in the nervous system. His arguably most influential contributions relate to the TAM RTKs Tyro3, Axl, and Mer, and their ligands Gas6 and Protein S. He and his colleagues demonstrated that these proteins together function as detectors of phosphatidylserine, the ‘eat-me’ signal through which dead (apoptotic) cells are recognized and engulfed by phagocytes. They further showed that the TAMs concomitantly act as feedback inhibitors of the innate immune response in macrophages, microglia, and other immune sentinels, and also facilitate infection of target cells by many enveloped viruses. In Alzheimer's disease, they demonstrated that microglia in the brain use the TAM system to construct dense-core amyloid plaques. As TAM-targeting drugs are already in patients, Dr. Lemke's work has immediate implications for the treatment of neurodegenerative, autoimmune, and oncologic diseases.