Naslov
The role of p53 and p73 genes in tumor formation

Autori
Moll, Ute M. ; Slade, Neda

Vrsta, podvrsta i kategorija rada
Poglavlja u knjigama, znanstveni

Knjiga
Handbook of Immunohistochemistry and in situ hibridization of human carcinomas. Vol 3: Molecular Genetics: Liver Carcinoma and Pancreatic Carcinoma

Urednik/ci
Hayat, M.A.

Izdavač
Academic Press

Godina
2005

Raspon stranica
103-117

ISBN
0-12-088404-6

Ključne riječi
p53, p73, tumor supressor, apoptosis, oncogene

Sažetak
The tumor suppressor p53 is critically important in the cellular damage response and is the ounding member of a family of proteins. All three genes regulate cell cycle and apoptosis after DNA damage. However, despite a remarkable structural and partly functional similarity among p53, p63, and p73, mouse knockout studies revealed an unexpected functional diversity among them. p63 and p73 knockouts exhibit severe developmental abnormalities but no increased cancer susceptibility, whereas this picture is reversed for p53 knockouts. Neither p63 nor p73 is the target of inactivating mutations in human cancers. Genomic organization is more complex in p63 and p73, largely the result of an alternative internal promoter generating NH2-terminally deleted dominant-negative proteins that engage in inhibitory circuits within the family. Deregulated dominant-negative p73 isoforms might play an active oncogenic role in some human cancers. Moreover, COOH-terminal extensions specific for p63 and p73 enable further unique protein-protein interactions with regulatory pathways involved in development, differentiation, proliferation, and damage response. Thus, p53 family proteins take on functions within a wide biological spectrum stretching from development (p63 and p73), DNA damage response via apoptosis and cell cycle arrest (p53, TAp63, and TAp73), chemosensitivity of tumors (p53 and TAp73), and immortalization and oncogenesis (DNp73).

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA