This article has multiple issues. Please help improve it or discuss these issues on the talk page. (Learn how and when to remove these messages)
|
Amy S. Lee | |
|---|---|
Amy Shiu Lee, 2013 | |
| Born | Guangdong, China |
| Education | University of California, Berkeley California Institute of Technology |
| Known for | Research on endoplasmic reticulum stress and GRP78/BiP |
| Awards |
|
| Scientific career | |
| Fields | Biochemistry Cancer biology |
| Workplaces | University of Southern California |
Amy S. Lee is a Chinese-born American biochemist and cancer biologist. She has served as Professor of Biochemistry and Molecular Medicine at the Keck School of Medicine of the University of Southern California (USC) from 1979 to 2025. Lee is best known for her pioneering research on endoplasmic reticulum (ER) stress and the discovery, regulation, and functions of the ER chaperone glucose-regulated protein 78 (GRP78), also known as BiP. Her work has been highly influential in elucidating the role of ER stress responses in development, cancer progression, therapeutic resistance, and viral infection. She served as Associate Director for Basic Research at the USC Norris Comprehensive Cancer Center from 1996 to 2019 and held the Judy and Larry Freeman Chair in Basic Science in Cancer Research. She has been Professor Emerita at USC since 2026.
Lee was born in Guangdong province in China, and grew up in Hong Kong. After high school in Hong Kong, she earned a Bachelor of Arts degree in Bacteriology and Immunology from the University of California, Berkeley, graduating as valedictorian in 1970. She subsequently attended the California Institute of Technology, where she received a Doctor of Philosophy degree in 1975.
Following postdoctoral training and service as a senior research associate at the California Institute of Technology, Lee joined the Department of Biochemistry at the Keck School of Medicine of USC in 1979 as an assistant professor. There, she established a research program focused on mammalian stress responses and molecular chaperones. Over the course of her career, she held multiple leadership roles at the USC Norris Comprehensive Cancer Center, including Director of the Gene Regulation Program (1987–1997), Associate Director for Basic Research (1996–2019), and Associate Director for Shared Resources (2020–2021).
Lee has also been recognized for her sustained commitment to mentoring graduate students, postdoctoral fellows, and junior faculty at USC.
Lee’s laboratory is the first to clone and characterize the mammalian genes encoding endoplasmic reticulum stress–inducible glucose-regulated proteins (GRPs). Her work helped define the transcriptional and post-transcriptional mechanisms governing GRP expression and established ER stress responses as central regulators of cellular homeostasis during development and disease.
A major focus of Lee’s research has been the ER chaperone GRP78, which she isolated in 1980. Her laboratory demonstrated that GRP78 plays a critical role in tumorigenesis, metastatic progression, and resistance to cancer therapies. She also reported that under conditions of cellular stress, GRP78 can relocalize from the ER to other cellular compartments, including the cell surface, where it functions as a co-receptor in oncogenic signaling pathways. Additionally, her group provided evidence that stress conditions can promote nuclear localization of GRP78, where it influences gene regulatory programs associated with cell migration and invasion. These findings challenged prevailing models of protein compartmentalization and expanded understanding of noncanonical chaperone functions in cancer.
During the COVID-19 pandemic, Lee’s laboratory investigated the role of GRP78 in viral infection. Her group reported that cell surface–localized GRP78 functions as a host co-receptor for SARS-CoV-2 entry and that ER-localized GRP78 is required for efficient viral protein folding and production. This work suggests that targeting GRP78 could have therapeutic potential against both cancer and viral pathogens that exploit ER stress pathways.