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 | Errol C. Friedberg
Department of Pathology, University of Texas Southwestern Medical Center at Dallas, Dallas, United States of America | | | Faculty Member: CELL BIOLOGY > Nuclear structure & function [ since 26 July 2001 ] |
| | [ Sponsorship ] [ Biography ] [ Homepage ] [ Evaluations ] | Sponsorship
Errol C. Friedberg sponsors free access to F1000 for De La Salle University, Manila, Philippines. Supporting F1000's initiative to make itself available to scientists in all countries, including free access to developing countries (more details). | Biography
Research interests:
The genome of all living organisms is subject to damage caused spontaneously or by exposure to environmental agents, which interact with DNA. Unrepaired DNA damage can result in permanent mutations and the most important phenotypic consequences of mutations in somatic cells are neoplastic transformation. My laboratory is interested in understanding the molecular mechanisms by which cells repair DNA damage and thereby mitigate against the development of cancer.
The yeast Saccharomyces cerevisiae is used as an eukaryotic model to explore the molecular biology and biochemistry of nucleotide excision repair (NER), a specific repair mode by which damaged bases are enzymatically excised from the genome. NER in yeast requires the products of at least 15 genes. A number of these genes are also required for RNA polymerase II transcription.
The hereditary human diseases xeroderma pigmentosum (XP) and Cockayne's syndrome (CS) are characterized by defective NER and by severe developmental and neurological dysfunction (CS), and a profound cancer predisposition (XP). In order to understand the molecular pathogenesis of these diseases we are studying cloned human genes directly to decipher their functional roles. Additionally we have constructed "knock-out" mouse strains carrying specific mutations, which mimic those present in human XP and CS patients. These mice offer the potential for phenotypic, biochemical and molecular studies on these diseases, and their relationship to cancer predisposition.
Finally, we have recently cloned mouse and human genes that are specifically required for the generation of spontaneous mutations in DNA. We are studying the function of these genes and their protein products and are constructing knock-out mice defective in these gene functions.
| Home page
http://www2.utsouthwestern.edu/gradschool/webrib/friedber.htm |
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