Stephen Elledge

Stephen Joseph Elledge ( born 1956 ) is an American geneticist and cancer researcher and professor at Harvard Medical School in Cambridge, Massachusetts.

Elledge is regarded as one of the leading researchers in the field of regulation of the cell cycle and the cellular response to genotoxic stress.

Life

Elledge earned a bachelor's degree in 1978 in chemistry at the University of Illinois and a Ph.D. in 1983 in biochemistry at the Massachusetts Institute of Technology (MIT). He worked from 1984 as a postdoctoral fellow at Stanford University. A first Assistant Professor of Biochemistry, he received in 1989 at Baylor College of Medicine in Houston, Texas, in 1995 a full professorship. After 14 years at Baylor College Elledge moving in 2003 to Harvard Medical School in Cambridge, Massachusetts. Since the same year he conducts research at the site of Brigham and Women's Hospital in Boston for the Howard Hughes Medical Institute ( HHMI ).

Work

At Stanford, Elledge discovered in his work via homologous recombination in eukaryotes happens to be a family of genes that encode Ribonukleotidreduktasen. He was able to show that these genes are activated by DNA damage. This activation may be used as markers for the cellular response to DNA damage. In Houston, he discovered the gene for CDK2 ( cyclin-dependent kinase 2, cyclin -dependent kinase 2 ), an enzyme that regulates the cell cycle transition from the G1 to the S phase and plays an important role in tumorigenesis. By means of a two-hybrid system was developed Elledge, he was able to identify several members of the CDK2 family of inhibitors together with Wade Harper, including p21 and p57. Mutations in p57 lead to Beckwith -Wiedemann syndrome, a disorder with tall stature and heaping tumors.

Elledge is known for his work on the effect of ubiquitin -mediated proteolysis on the proteome. He was able to identify F- box proteins that regulate protein degradation in the cell, because they highlight proteins target sequences with ubiquitin, after which the degradation follows by proteasomes. Ultimately, the family of ubiquitin - Cullin ligases could be described.

Recent work dealing with genetic studies of the mechanisms responsible for the cellular detection of DNA damage or cancer based. Together with Gregory Hannon ( Cold Spring Harbor Laboratory ) has created Elledge libraries of mouse and human- shRNA ( short hairpin RNA). In the sequence, a number of tumor suppressors and proteins could be identified, the survival of which depends exclusively presence of tumor cells. This led to the concept of non -oncogene addiction (NOA, non- oncogenic dependence).

Awards (selection)

Cambridge (Massachusetts) Genetic recombination Beckwith–Wiedemann syndrome Small hairpin RNA Gairdner Foundation International Award Digital Object Identifier
304401
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