The old and the new in p53 functional regulation.
The gene termed p53 is one of the most extensively studied for the past 18 years and the amount of literature published on this gene reflects its relevance in the field of molecular oncology; thus, loss or mutation of this oncosuppressor gene is probably the molecular lesion most frequently observed in human tumors. The aim of this minireview is to report, discuss, and interpret some recent observations on this topic: (I) The relationship with the Ataxia-Telangectasia gene and with the signaling enzyme phosphatidylinositol 3-kinase (PI3K). (II) The relationship between DNA damage, p53, and sensitivity to anticancer therapies. (III) The gain of function caused by mutations that transform the oncosuppressor p53 gene into a dominant transforming oncogene and (IV) The phosphorylative regulation of p53 and its relationship with the mitogenic signaling cascade involving protein kinase C and tumor promoters.
Magnelli
L
L
Laboratory of Molecular Biology at the Institute of General Pathology, University of Florence , Viale Morgagni 50, Florence, 50134, Italy.
Ruggiero
M
M
Chiarugi
V
V
D001260:Ataxia Telangiectasia / Q000235:genetics; D004249:DNA Damage; D016158:Genes, p53 / Q000502:physiology*; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation; D011493:Protein Kinase C / Q000502:physiology
D019869:Phosphatidylinositol 3-Kinases; D011493:Protein Kinase C