Journal of Leukemia

Journal of Leukemia
Open Access

ISSN: 2329-6917

+44 1202068036

David Reisman

David Reisman

David Reisman
Professor, Department of Biological Sciences
University of South Carolina, USA

Biography

DAVID REISMAN (Ph.D., University of Wisconsin–Madison, 1986) is a Professor of Biological Sciences in the College of Arts and Sciences at the University of South Carolina, Columbia and the Director of the Center for Colon Cancer Research Tissue Biorepository. He received his BS degree in Biology and MS degree in Plant Virology from the University of Illinois - Urbana. Prior to joining USC in 1991 he was a Post-doctoral Fellow at the Weizmann Institute of Science (Rehovot, Israel) as well as the University of Colorado – Boulder. His research deals with understanding the regulation of the p53 Tumor Suppressor gene and has published over 45 research articles many of which are in high impact journals such as the Journal of Biological Chemistry, Oncogene, Molecular and Cellular Biology, and Cancer Research. Over the years he has received grant funding from the American Cancer Society, National Institutes of Health, the US Department of Defense, the Wendy Will Case Cancer Fund, and the Elsa U. Pardee Cancer Fund. He has served on Scientific Advisory/Grant Review Study Sections for the American Cancer Society, the National Institutes of Health, Susan G. Komen Breast Cancer Foundation, the Beckman Undergraduate Research Foundation and co-chaired the USC Magellan Undergraduate Research Award Panel. He was received the 2000 College of Science and Mathematics Outstanding Advisor Award, the 2003 Michael J Mungo Teaching Award, the 2010 Distinguished Undergraduate Research Mentor Award, and the USC Mortar Board Excellence in Teaching Award in 2008 and 2011.

Research Interest

p53 is a DNA-binding transcription factor that activates genes responsible for a cell cycle checkpoint or apoptosis after exposure to ionizing radiation, UV light or other DNA damaging agents. The p53 protein is induced both in terms of its abundance and its activity in response to DNA damage. Increased levels of p53 protein are largely due to increased stability of the protein that is regulated through the loss of association with the MDM2 protein. In normal cells were p53 is found at very low levels, p53 is present in a complex with MDM2 which targets p53 for degradation through the ubiquitin pathway. Defects in the p53 pathway are the most common genetic aberration seen in human cancers. It has been known for quite some time that the level of p53 is increased at the transcriptional level after growth factor stimulation of resting murine and human lymphocytes and resting fibroblasts. Induced expression of p53 prior to S-phase appears to serve as a mechanism for providing a rapid response to DNA damage during S-phase. In previous studies we found that that the transcriptional regulator, RBP-J, an essential target of the Notch receptor signaling pathway, binds to the p53 promoter in a cell-cycle regulation fashion and serves to repress p53 gene expression in G0 while the transcription factor C/EBP2 binds to the same site on the p53 promoter in response to mitogen stimulation and serves to increase p53 promoter expression as cells enter S-phase. It is becoming increasingly clear that deregulated transcription of the p53 gene, both increased and decreased, can contribute to human cancer as there are now numerous examples among tumors in which transcription of the mutant p53 gene was shown to be enhanced while expression of the wild-type gene is reduced or absent leading to the functional elimination of wild type p53.

Top