|Education||MS, Johns Hopkins University|
p53 is a tumor suppressor that is commonly mutated in diverse cancers. When activated in response to chromosomal DNA damage, p53 is stabilized in the nucleus and thereupon initiates a complex transcriptional program that regulates cell cycle arrest, senescence, and apoptosis. The response of p53 to DNA damage has been extensively characterized; however, p53 also has a role in in the cellular defenses against pathogens that remains poorly understood. Gaining greater insight into the mechanism by which p53 is capable of modulating fundamental mechanisms of innate immunity may provide insight into the mechanisms by which immune deficiencies arise during tumorigenesis. The goal of my research is to use newly generated viral mutants in parallel with novel mutant human cell lines in order to elucidate the mechanisms by which p53 orchestrates the innate immune response.
Miciak J, Bunz F. Long story short: p53 mediates innate immunity. Biochim Biophys Acta. 2016 Mar 4;1865(2):220-227. doi: 10.1016/j.bbcan.2016.03.001. [Epub ahead of print] Review. PMID: 26951863