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Oncology Experts

Junying Yuan

Scientist
Ludwig Center at Harvard
Ludwig Institute for Cancer Research
United States of America

Biography

I have made several critical contributions to our understanding of apoptosis and necroptosis, which regulate the survival of mammalian cells. As a graduate student at the Harvard Medical School, working in the laboratory of H. Robert Horvitz at the Massachusetts Institute of Technology, I helped uncover the first described mechanism of programmed cell death in the nematode C. elegans. Later, while at the Cardiovascular Research Center, Massachusetts General Hospital, I demonstrated that an enzyme later named caspase-1 is a functional homologue of C. elegans cell death gene product Ced-3 and that its inhibition can block neuronal cell death. After moving to the Department of Cell Biology at Harvard Medical School, where I am today Professor of Cell Biology, my lab discovered and analyzed necroptosis, a regulated necrotic cell death mechanism. This disproved the prevailing belief that necrosis is a kind of unregulated, passive cell death. My lab continues to probe cell death and is exploring strategies to reduce the lethal accumulation of misfolded proteins within cells. A small molecule inhibitor of RIPK1 kinase (Nec-1) we discovered is now in preparation for a clinical trial for neurodegenerative disease. I have received many honors and awards for my work and am a Fellow of both the American Academy of Arts and Sciences and the American Association for Advancement of Sciences.

Research Interest

Cancer cell biology, cancer therapeutics, apoptosis and necroptosis

Publications

  • Yuan, Junying, and Bruce A. Yankner. "Apoptosis in the nervous system." Nature 407.6805 (2000): 802.

  • Klionsky, Daniel J., et al. "Guidelines for the use and interpretation of assays for monitoring autophagy." Autophagy 12.1 (2016): 1-222.

  • Alnemri, Emad S., et al. "Human ICE/CED-3 protease nomenclature." Cell 87.2 (1996): 171.

  • Li, Honglin, et al. "Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis." Cell 94.4 (1998): 491-501.

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