Defects in 'orphan' inositol polyphosphates may be linked to manic depression, cancer

Lithium has been effective in the treatment of bipolar or manic depressive disease for more than 40 years yet scientists still don't understand fully how it works, that is, what target in the cell the lithium hit once it began circulating in the blood. Without this information, it is difficult to know how to create other, perhaps more effective drugs, or drugs that will work for patients who do not respond to lithium. A scientist who provided important insights into possible targets of lithium - and this year's recipient of the American Society for Biochemistry and Molecular Biology's Schering Plough Award -- will describe his current research on April 21 at the Experimental Biology 2002 meeting in New Orleans.

Dr. John D. York, Howard Hughes Medical Institute Assistant Investigator, Duke University Medical Center, focuses on the elucidation of communication pathways between cells - a process called signaling - and the mechanisms by which defects in these pathways may lead to diseases such as manic depression and cancer.

Dr. York is perhaps best known for identifying biological roles for "orphan" intracellular signaling molecules known in general as inositol polyphosphates, a discovery which changed how scientists regard inositol signaling and its possible impact on disease and the design of new therapies.

His own previous work illustrates the impact of these little understood molecules. As a graduate student, Dr. York took apart the three dimensional structure of inositol polyphosphate 1-phosphatase, an enzyme that many scientists suspected was the target of lithium. At the center of the enzyme he found and was able to characterize a unique structure he then used as a guide to identifying other enzymes that could serve as additional targets for lithium. This work also may provide the basis for the design of more specific drugs that may not have the negative side effects some patients experience on lithium. He found that lithium inhibits s

Contact: Sarah Goodwin
Federation of American Societies for Experimental Biology

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