In unstressed cells, the p53 tumor suppressor is highly unstable. DNA damage and other
forms of cellular stress rapidly stabilize and activate p53. This process is regulated by a
complex array of post-translational modifications that are dynamically deposited onto p53.
Recent studies show that these modifications orchestrate p53-mediated processes such as
cell cycle arrest and apoptosis. Cancer cells carry inherent genetic damage, but avoid arrest
and apoptosis by inactivating p53. Defining the enzymatic machinery that regulates the …