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Background: p53 acts as both a tumor-suppressor and transcription factor that, upon activation by DNA damage and other cellular stress signals, leads to the transcription of genes triggering cell-cycle arrest, apoptosis, and DNA repair (1,2). The gene for the nuclear phosphoprotein p53 is the most commonly mutated gene yet identified in human cancers (3). p53 is frequently mutated or inactivated in about 60% of cancers. Due to UV-induced DNA damage, p53 is phosphorylated on eight different serine/threonine locations on the N-terminal. Phospholyation on serine 46 has been implicated as a mediator in apoptosis induced by DNA-damage (4, 5).