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Pregled bibliografske jedinice broj: 206201

P63 and p73: Roles in development and tumor formation. Mol Cancer Res (2004) 2: 371-386


Moll, Ute M.; Slade, Neda
p63 and p73: Roles in development and tumor formation. Mol Cancer Res (2004) 2: 371-386 // Molecular cancer research, 2 (2004), 371-386 (međunarodna recenzija, pregledni rad, znanstveni)


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Naslov
P63 and p73: Roles in development and tumor formation. Mol Cancer Res (2004) 2: 371-386
(P63 and p73: Roles in development and tumor formation. Mol Cancer Res (2004) 2: 371-386.)

Autori
Moll, Ute M. ; Slade, Neda

Izvornik
Molecular cancer research (1541-7786) 2 (2004); 371-386

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, pregledni rad, znanstveni

Ključne riječi
p53; p73; DNA damage; apoptosis; chemosensitivity

Sažetak
The tumor suppressor p53 is critically important in the cellular damage response and is the founding 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 (delta Np73).

Izvorni jezik
Engleski

Znanstvena područja
Biologija, Temeljne medicinske znanosti



POVEZANOST RADA


Projekti:
0098092

Ustanove:
Institut "Ruđer Bošković", Zagreb

Profili:

Avatar Url Neda Slade (autor)


Citiraj ovu publikaciju

Moll, Ute M.; Slade, Neda
p63 and p73: Roles in development and tumor formation. Mol Cancer Res (2004) 2: 371-386 // Molecular cancer research, 2 (2004), 371-386 (međunarodna recenzija, pregledni rad, znanstveni)
Moll, U. & Slade, N. (2004) p63 and p73: Roles in development and tumor formation. Mol Cancer Res (2004) 2: 371-386. Molecular cancer research, 2, 371-386.
@article{article, year = {2004}, pages = {371-386}, keywords = {p53, p73, DNA damage, apoptosis, chemosensitivity}, journal = {Molecular cancer research}, volume = {2}, issn = {1541-7786}, title = {p63 and p73: Roles in development and tumor formation. Mol Cancer Res (2004) 2: 371-386}, keyword = {p53, p73, DNA damage, apoptosis, chemosensitivity} }
@article{article, year = {2004}, pages = {371-386}, keywords = {p53, p73, DNA damage, apoptosis, chemosensitivity}, journal = {Molecular cancer research}, volume = {2}, issn = {1541-7786}, title = {p63 and p73: Roles in development and tumor formation. Mol Cancer Res (2004) 2: 371-386.}, keyword = {p53, p73, DNA damage, apoptosis, chemosensitivity} }

Časopis indeksira:


  • Current Contents Connect (CCC)
  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE


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  • Chemical Abstracts
  • Index Medicus
  • BIOSIS Previews
  • MEDLINE





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