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Mutation of the p53 tumor suppressor gene is the most frequent lesion detected in cancer. Consequently, understanding the structure and function of the normal p53 protein and how it differs from the mutant p53 proteins that are commonly found in cancer patients' tumors should provide valuable information. When cells are induced to accumulate high levels of p53 by agents of stress such as DNA damage or hypoxia, they either undergo cell cycle arrest or programmed cell death. We and others have shown that p53 is a binding protein that can activate transcription from reporter templates bearing p53 binding sites. We have analyzed in detail the functional domains of p53 and how they are regulated by both covalent and non-covalent modifiers. A number of p53 t arget genes have been identified whose functions are relevant to cell arrest or apoptosis. However, in some cases p53 induces apoptosis in a transactivation-independent manner. Although p53 is widely studied there are several questions that remain about this important protein: How do cells transmit signals from genotoxic stress to activate p53? What are the downstream targets of p53 that are involved in its many functions in cells? What is the transactivation-independent function of p53 and how does it work? Finally, with respect to the central role that p53 plays in human cancer, can we use information derived from the basic research on this protein to develop p53-based cancer therapeutics? The search for answers to these and other questions are the basis for much of the work currently going on in our laboratory.
The cell cycle of higher eykaryotes requires the activity of a number of cyclin dependent protein kinases (CDKs). Although information has accumulated about how the CDKs themselves are regulated, less is known about the substrates of these enzymes whose phosphorylation leads to cell cycle regulation. An ongoing project in our laboratory is the study of a number of CDK substrates and how phosphorylation regulates their function. We are particularly interested in how CDKs affect DNA synthesis and DNA repair.
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Gizem Efe,Katherine Cunningham, Raul Navaridas Fernandez de Bobadilla,Karen J. Dunbar,Kensuke Sugiura, Noriyuki Nishiwaki,Saul Carcamo,Lois Resnick-Silverman,Dan Hasson,Andres J. Klein-Szanto,Alison M. Taylor,James J. Manfredi,Carol Prives,Anil K. Rustgi
Cancer Researchno. 6_Supplement (2024): 1270-1270
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#Papers: 265
#Citation: 32441
H-Index: 78
G-Index: 180
Sociability: 7
Diversity: 0
Activity: 2
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