Reed B. Wickner (born c. 1942) is an American yeast geneticist. In 1994 he proposed that the [PSI+] and [URE3][1] phenotypes in Saccharomyces cerevisiae, a form of budding yeast, were caused by prion forms of native proteins - specifically, the Sup35p and Ure2p proteins, respectively.
Reed Wickner | |
|---|---|
| Born | About 1942 |
| Education | Cornell University (B.A.) Georgetown University (M.D) |
| Known for | Work on prions and amyloid diseases |
| Scientific career | |
| Fields | Yeast genetics |
| Institutions | National Institute of Diabetes & Digestive & Kidney Diseases, National Institutes of Health |
Wickner graduated from Cornell University with a B.A. degree in 1962. He then went to medical school at Georgetown University and received his M.D. degree in 1966. He is a member of the National Academy of Sciences (NAS), the American Academy of Arts and Sciences [(AAAS)],[2] and the American Academy of Microbiology, and has been a fellow of the American Association for the Advancement of Science. He is (as of 2012) Chief of the Laboratory of Biochemistry and Genetics at the National Institute of Diabetes & Digestive & Kidney Diseases, part of the National Institutes of Health. His research interests pertain to prions and amyloid diseases.
References
edit- ^ [URE3] as an altered URE2 protein: evidence for a prion analog in Saccharomyces cerevisiae. Science. 1994 Apr 22; 264(5158): 566-9 Abstract
- ^ "AAAS Honors Three from NIH"
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