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Victor Ambros

Victor R. Ambros
Victor Ambros.jpg
Victor Ambros (Photo: Jane Gitschier)
Born (1953-12-01) December 1, 1953 (age 63)
Hanover, New Hampshire
Fields Biology
Institutions M.I.T. Center for Cancer Research (1975-1976)
Massachusetts Institute of Technology (1976-1979)
Harvard University(1985-1992)
Dartmouth College(1992-2001)
Dartmouth Medical School (2001-2007)
University of Massachusetts Medical School (2008-)
Alma mater Massachusetts Institute of Technology (B.S., 1975) (Ph.D., 1979)
Known for discovery of the first known microRNA

Victor R. Ambros (born 1953, Hanover, New Hampshire) is an American developmental biologist who discovered the first known microRNA (miRNA). He is a professor at the University of Massachusetts Medical School in Worcester, Massachusetts.

Ambros was born in New Hampshire. His father was a Polish war refugee and Victor grew up on a small dairy farm in Vermont in a family of eight children. He received his BS in Biology from the Massachusetts Institute of Technology in 1975 and completed his PhD in 1979 at the Massachusetts Institute of Technology, under the supervision of Nobel laureate David Baltimore. Ambros continued his research at MIT as the first postdoctoral fellow in the lab of future Nobel laureate H. Robert Horvitz. He became a faculty member at Harvard University in 1984 and moved to Dartmouth College in 1992. Ambros joined the faculty at the University of Massachusetts Medical School in 2008, and currently holds the title of Silverman Professor of Natural Sciences in the program in Molecular Medicine.

In 1993, Ambros and his co-workers Rosalind Lee and Rhonda Feinbaum reported in the journal Cell that they had discovered single-stranded non-protein-coding regulatory RNA molecules in the organism C. elegans. Previous research, including work by Ambros and Horvitz, had revealed that a gene known as lin-4 was important for normal larval development of C. elegans, a nematode often studied as a model organism. Specifically, lin-4 was responsible for the progressive repression of the protein LIN-14 during larval development of the worm; mutant worms deficient in lin-4 function had persistently high levels of LIN-14 and displayed developmental timing defects. However, the mechanism for control of LIN-14 remained unknown.


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