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| Name |
Cleaver, James E. |
| Location
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University of California, San Francisco |
| Primary Field
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Medical Genetics, Hematology and Oncology |
| Secondary Field
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Genetics |
 Election Citation
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Cleaver discovered the genetic defects in the initial steps of DNA excision repair in the human disease, xeroderma pigmentosum, and paved the way for using this class of diseases to characterize the basic molecular biology of DNA repair in human cells. |
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Research Interests
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All genomes contain numerous genes whose primary role is preserving the stability of the genome. These genes regulate various cellular responses involving DNA repair, cell cycle progression, cell division, and signal transduction after exposure to chemicals and radiations from internal or external sources. The proteins encoded by these genes are often involved in several different repair systems, as well as in other basic transcription, replication, and recombination process that can be separate from their roles in repair. The first connection between DNA damage, DNA repair, and human genetic predisposition to cancer came with my discovery of the cause of human hereditary disease, xeroderma pigmentosum. The concept that specific mechanisms control genetic stability that developed from this work now permeates much of cancer research and has had impact far beyond its beginnings in a rare human hereditary disease of sunlight-induced skin cancer. My current interest lies in understanding how repair of different kinds of DNA damage is achieved by transient multiprotein complexes composed of interchangeable components and how organisms from the three major kingdoms evolved similar paradigms for achieving genetic stability. |
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