Activation of p53 sequence-specific DNA binding by short single strands of DNA requires the p53 C-terminus

Article Abstract:

Short single stranded DNA nucleotides having 16-40 nucleotides can stimulate the binding of human and murine p53 proteins to a p53 response element in supercoiled DNA but not the binding of a split p53 in which the C-terminal is missing. The p53 tumor suppressor protein which is activated when DNA is damaged, has an activation center, a DNA binding domain and an oligomerization domain. p53 activates many genes when the concentration of DNA damaging agents is high.

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Splicing into senescence: The curious case of p16 and p19ARF

Article Abstract:

The cyclin-dependent kinase inhibitor p16 is implicated in cell cycle regulation and cellular senescence, and its loss leads to a genetic predisposition to malagnant melanoma and pancreatic cancer. Its discovery was the result of advances in cancer genetics and cell cycle regulation, and was linked to the discovery of genomic deletions. P19ARF is a novel transcript with an identical 3' sequence to p16, but with a unique 5' end.

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Selective evolution of stromal mesenchyme with p53 loss in response to epithelial tumorigenesis

Article Abstract:

Tumor-suppressor gene mutations within the stroma in some human carcinomas are analyzed. The results showed that the interplay among multiple cell types select for aberrations nonautonomously during tumor progression, where the interaction imposes strong selective pressure yielding a highly proliferative mesenchyme that has undergone p53 loss.

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