Cellular DNA damage causes stabilization and activation of the tumor suppressor and
transcription factor p53, in part by promoting multiple covalent modifications of the p53 …

Activation of p53-mediated transcription is a critical cellular response to DNA damage. p53
stability and site-specific DNA-binding activity and, therefore, transcriptional activity, are …

The p53 tumor suppressor is a sequence-specific transcription factor that undergoes an
abundance of post-translational modifications for its regulation and activation. Acetylation of …

The tumor suppressor p53 exerts antiproliferation effects through its ability to function as a
sequence-specific DNA-binding transcription factor. Here, we demonstrate that p53 can be …

Post-translational modifications of p53 are critical in modulating its tumor suppressive
functions. Ubiquitylation, for example, plays a major role in dictating p53 stability, subcellular …

p53 promotes tumor suppression through its ability to function as a transcriptional factor and
is activated by posttranslational modifications that include acetylation. Our earlier study …

The activity of the p53 gene product is regulated by a plethora of posttranslational
modifications. An open question is whether such posttranslational changes act redundantly …

p53, the most commonly mutated gene in cancer cells, directs cell cycle arrest or induces
programmed cell death (apoptosis) in response to stress. It has been demonstrated that p53 …

Acetylation of multiple lysine residues in the p53 plays critical roles in the protein stability
and transcriptional activity of p53. To better understand how p53 acetylation is regulated, we …

Cell-cycle arrest, apoptosis, and senescence are widely accepted as the major mechanisms
by which p53 inhibits tumor formation. Nevertheless, it remains unclear whether they are the …