Ricerca di Base P63

 

INTRODUCING P63
In 1998, both the human and mouse orthologues of a p53-related gene were identified and named p63 (Kaghad, Bonnet et al. 1997). The human cDNAs previously cloned independently by other groups encoding p53 homologues named p51, p40, p73L and CUSP, as well as the partial cDNA previously identified encoding a rat p53 homologue called KET, revealed themselves all alternative mRNAs from the p63 gene (Irwin and Kaelin 2001).
The p53 family is completed  by p73, identified in 1997 (Kaghad, Bonnet et al. 1997). Despite the significant amino acid identity between the three members, and the fact that they are all able to bind to the canonical p53 DNA responsive element (5’ PuPuPuCA/TT/AGPyPyPy 3’) they appear to play quite different roles. p53 is the principal tumor-suppressor gene, being mutated in 50% of human cancers (Levine 1997), and a key regulator of the cell cycle, allowing completion of genomic-repair processes before division, to prevent damaged cells to become uncontrolled (Caspari 2000). As it is well known from literature, p63 and p73 do not represent classical tumor-suppressor genes. Rather, they act as key regulators in development – p73 in neuronal and pherormonal pathways (Kaghad, Bonnet et al. 1997) – and p63 in limb, epithelial and craniofacial development (Kaghad, Bonnet et al. 1997; Ihrie, Marques et al. 2005, Viganò and Mantovani 2007).

 

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Roberto Mantovani
Dipartimento di Scienze biomolecolari e Biotecnologie
Università degli Studi di Milano
Via Celoria 26, 20133 Milano, Italia
Tel.02-50315011
mantorlab.unimi.it