Review article
The p53 family of genes in development and tumor formation
Arijana Zorić
; Department of molecular medicine, Laboratory for molecular oncology, Ruđer Bošković Intitute, Zagreb, Croatia
Anđela Horvat
; Department of molecular medicine, Laboratory for molecular oncology, Ruđer Bošković Intitute, Zagreb, Croatia
Neda Slade
orcid.org/0000-0003-3620-3099
; Department of molecular medicine, Laboratory for molecular oncology, Ruđer Bošković Intitute, Zagreb, Croatia
Abstract
TP53 tumor suppressor protein is crucial in the cell growth control and the maintenance of genomic stability. These activities are due, at least in part, to its ability to form homooligomers that bind to specifi c DNA sequences and acti vate transcripti on. Later discovered
p53 homologues, p63 and p73 share remarkable structural and partly functional similarity with p53. All three genes have two promoters and undergo alternative splicing to generate multiple isoforms that might play important roles in carcinogenesis. Both p63 and
p73 genes generate two groups of isoforms: transacti vati ng forms (TAp63/73) with tumor suppressor activities as well as a number of N-terminally truncated transactivation- deficient transdominant isoforms (called ΔNp63/73). It was recently discovered that p53, like
p73, has a second internal promoter that leads to the synthesis of multiple isoforms whose function is not yet fully clear. In this review different isoforms of p63, p73, p53 and their roles in development and tumorigenesis are described. Defining the interacti ons between
p53/p63/p73 would give a new insight into the roles of these proteins in tumorigenesis.
Keywords
development; differentiation; p53; p63; p73; tumorigenesis
Hrčak ID:
53158
URI
Publication date:
7.6.2010.
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