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Scientists develop chemical switch for natural signaling molecules, opening new approach to biomedical research and drug design

Applying the tools of chemistry where modern genetic techniques have so far fallen short, a team led by a University of California, San Francisco scientist has developed drug-like inhibitors to study vital signaling molecules essential for almost all cell activity. The research opens the way to identify the functions of hundreds of these molecules, called kinases, crucial to signal transmission in all cells and, in the same step, identify precisely how drugs can inhibit kinases when they go awry and cause disease.

In the current (September 21) issue of the journal Nature, the scientists reported first using genetic techniques to carve out a small part of a kinase molecule - a constituent common to the many hundred known kinases. They then searched for small molecules that fit precisely into the pocket created by this structural change. The added molecule inhibited, but did not destroy kinase function -- just what is needed to tease apart the unique role of one kinase from all others.

The new technique can chemically switch on or off individual kinases among many hundreds found in every cell. Until now, changing the structure of proteins to study their function has been the hallmark of modern molecular genetics, leading to fundamental leaps of understanding, including the identification of tumor-suppressor genes and their role in cancer. But essential as they are to nearly all life processes, kinases have proven resistant to genetic approaches to study them.

"Instead of trying to figure out what was unique to each of the hundreds of kinases, we looked for what was common to all of them," explained Kevan Shokat, PhD, UCSF associate professor of cellular and molecular pharmacology and senior author on the research paper. "We then used a genetic mutation to carve a new hole in this common, active site of the kinase and introduced a new molecule which specifically bound to the pocket we created."
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Contact: Wallace Ravven
wravven@pubaff.ucsf.edu
415-476-2557
University of California - San Francisco
24-Sep-2000


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