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The p53 gene is mutated in at least half of all human cancers, underscoring its critical role in tumor suppression. p53 is a cellular stress sensor, responding to diverse insults such as DNA damage, hyperproliferative signals, and hypoxia by inducing growth arrest or apoptosis, responses thought to be important to tumor suppression. In addition, as a cellular stress sensor, p53 plays both physiological and pathological roles beyond tumor suppression. For example, p53 plays beneficial roles such as promoting fertility and pigmentation, as well as inducing detrimental phenotypes in certain situations such as the side effects of cancer therapies or the cell death observed during stroke or neurodegenerative disease. The overarching goal of our research is to better define the mechanisms by which the p53 protein promotes different responses in different settings, ranging from tumor suppression to responses to chemotherapeutics, using the mouse as an in vivo model system. We utilize a combination of mouse genetic, cell biological, and genomic approaches to address these questions. For example, we have generated p53 knock-in mutant mice to investigate the contribution of particular p53 activities to p53 function in vivo as well as knockout mice lacking specific p53 target genes to examine the function of specific p53 target genes in p53 pathways in vivo. In addition, we utilize genomic technologies including ChIP-sequencing and RNA-sequencing to elucidate the genes activated and repressed by p53 in diverse settings. Using these combined approaches, we aim to decipher the molecular activities relevant for p53 action in different contexts and to define transcriptional networks responsible for mediating p53 function in a variety of different processes.

We can be found in CCSR-1240 South
Stanford University Medical Center
269 Campus Drive
Stanford, CA 94305-5152
ph 650-723-5261
fax 650-723-7382

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