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Charles Brenner, Ph.D.
Title(s):
Professor of Genetics and of Biochemistry
Associate Director for Basic Sciences, Norris Cotton Cancer Center
Department(s):
Biochemistry
Genetics
Education:
B.A., Biology, Wesleyan University (1979-1983)
Ph.D., Cancer Biology, Stanford University School of Medicine (1988-1993)
Postdoctoral, X-ray Crystallography, Brandeis University (1993-1996).
Programs:
Molecular and Cellular Biology Graduate Programs
Norris Cotton Cancer Center
Websites:
http://www.dartmouth.edu/~brenner/
http://www.cancer.dartmouth.edu/members/brenner.shtml
Contact Information:
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Dartmouth Medical School Rubin 733--HB7937 Lebanon NH 03756 |
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Office: Rubin 733 Phone: 603-653-9922 Fax: 603-653-9923 Email: Charles.Brenner@Dartmouth.edu Assistant: Andrea Tillotson Asst. Phone: 603-653-3626 Asst. Email: andrea.l.tillotson@dartmouth.edu |
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Selected Publications: |
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P. Bieganowski & C. Brenner Discoveries of Nicotinamide Riboside as a Nutrient and Conserved NRK Genes Establish a Preiss-Handler Independent Route to NAD+ in Fungi and Humans. Cell v. 117, pp. 495-502, 2004 (view details on MedLine) P. Belenky, F.G. Racette, K.L. Bogan, J.M. McClure, J.S. Smith & C. Brenner Nicotinamide Riboside Promotes Sir2 Silencing and Extends Lifespan via Nrk and Urh1/Pnp1/Meu1 Pathways to NAD+ Cell v. 129, pp. 473-484, 2007 (view details on MedLine) G.L. Loring, K.C. Christensen, S.A. Gerber & C. Brenner Yeast Chfr Homologs Retard Cell Cycle at G1 and G2/M via Ubc4 and Ubc13/Mms2-Dependent Ubiquitination. Cell Cycle v. 7, pp. 95-105, 2008 (view details on MedLine) |
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Professional Interests:
The Brenner laboratory has three research interests, each of which is related to cell cycle and metabolism in cancer and aging.
First, we study the function of the Fhit tumor suppressor protein, which is lost early in the development of epithelial tumors in carcinogen-exposed tissues such as the lung. We have discovered early gene expression consequences of loss of Fhit from immortalized bronchial epithelia and are dissecting the mechanisms by which these genes become dysregulated.
Second, we cloned the two yeast homologs of Chfr, which is another tumor suppressor lost in epithelial malignancies. We have discovered several additional genes required for Chf1 and Chf2 to arrest the yeast cell division cycle at two stages. Additionally, with our colleague Scott Gerber, we developed quantitative methods to characterize the function of Chf1 and Chf2 as RING E3 ubiquitin ligases.
Third, we have discovered unanticipated vitamins, metabolites, metabolic processes and regulation in eukaryotic NAD biosynthesis that are altered by calorie restriction and that have the potential to improve human health. We are currently dissecting new regulatory mechanisms in yeast and testing effects of nicotinamide riboside in vertebrate cells.
Courses Taught:
Genetics 44/144 Oncogenomics
Grant Information:
1997-2008 NIH R01 CA075954, "Functional and Structural Analysis of HIT Proteins"
2007-2011 NIH R01 CA081665, "Quantitative Analysis of RING E3 Ubiquitin Ligases"
2008-2011 NSF MCB-0822581, New Steps in NAD+ Metabolism
2008-2009 Lung Cancer Research Foundation Award
Copyright © 2009 Trustees of Dartmouth College