This is from the online Wikepedia:
p53 (also known as
protein 53 or
tumor protein 53), is a
transcription factor which in humans is encoded by the
TP53 gene.
[1][2][3] p53 is important in
multicellular organisms, where it regulates the
cell cycle and thus functions as a
tumor suppressor that is involved in preventing
cancer. As such, p53 has been described as "the guardian of the
genome," "the guardian angel gene," and the "master watchman," referring to its role in conserving stability by preventing genome mutation.
[4]
The name p53 is in reference to its apparent
molecular mass: it runs as a 53
kilodalton (kDa) protein on
SDS-PAGE. But based on calculations from its
amino acid residues, p53's mass is actually only 43.7kDa. This difference is due to the high number of
proline residues in the protein which slow its migration on
SDS-PAGE, thus making it appear heavier than it actually is.
[5] This effect is observed with p53 from a variety of species, including humans, rodents, frogs, and fish.
Mutations that deactivate p53 in cancer usually occur in the DBD. Most of these mutations destroy the ability of the protein to bind to its target DNA sequences, and thus prevents transcriptional activation of these genes. As such, mutations in the DBD are
recessive loss-of-function mutations. Molecules of p53 with mutations in the OD dimerise with
wild-type p53, and prevent them from activating transcription. Therefore OD mutations have a dominant negative effect on the function of p53.
It would seem that overexpression of a mutant form of p53, 2nd paragraph above, could play a role. You'd want to double check this, but this would make logical sense. The references above are from Wikepedia, just google p53 expression tumor and click on the wikepedia site.
