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The p53 tumour suppressor gene represents the most common target for mutational inactivation in human cancer. At the cellular level, p53 protein regulates cell cycle progression, senescence, apoptosis and various metabolic processes. p53 is a sequence-specific DNA-binding transcription factor. In response to abnormal proliferative signals and many stress signals including DNA damage, p53 protein is stabilized and activated through a succession of post-translational modifications including phosphorylation and acetylation. Once activated, p53 regulates the expression of a number of target coding genes and non-coding RNAs that collectively contribute to p53-dependent cellular responses. p53 protein can induce cells to undergo a transient arrest in the G1 phase of the cell cycle that is believed to allow time for repair of damaged DNA before the initiation of S phase. Activated p53 can also eliminate cells through mechanisms that involve prolonged arrest in G1 (senescence) or apoptosis. The elimination of damaged, stressed or abnormally proliferating cells by p53 explains in part the tumour suppression function of p53.
My research program has three goals:
1. To understand how the p53 protein regulates cell growth and suppresses tumorigenesis.
2. To evaluate the role of p53 as a determinant of chemosensitivity in cancer cells.
3. To understand how DNA replication stress contributes to premature cellular senescence, aging, and p53 activation.
p53 Tumour Suppressor Gene, Apoptosis, Senescence, Cancer and Progeria