Recently, I heard an interesting talk by Arnold Levine about the p53
suppressor gene and it's function. He proposed that the p53 gene product
is responsible for recognizing damaged DNA which would subsequently
result in one of two pathways: cell cycle arrest or apoptosis depending
on where the cell was in the cell cycle and possibly the cell type (eg
thymocytes/apoptosis).
I wasn't sure how the pivotal role of the p53 gene products and the cell
cycle interacted with ongoing repair of DNA by the DNA repair enzymes.
Does anyone know?
Is it known if there are defects in the DNA repair
enzymes associated with defects in p53 leading to a greater incidence
of carcinoma?
Why would a cell chose to arrest at G1 instead of
apoptosing in the face of damaged DNA and mutations?
Michelle
