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Conquering the complexity of p53

New evidence from a Trp53 'knock-in' mouse model suggests that p53-dependent cell cycle checkpoint control accompanied by maintenance of genome stability is important for keeping tumor growth in check.

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Figure 1: A number of cellular stresses, including DNA damage, hypoxia and hyperproliferative signals, activate p53 to stimulate target gene expression.

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Attardi, L., DePinho, R. Conquering the complexity of p53. Nat Genet 36, 7–8 (2004). https://doi.org/10.1038/ng0104-7

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