The DOI matches its Crossref record; 165 of the 165 references it cites were found in a registry or an index.
p63 and p73: Roles in Development and Tumor Formation
Open accessAbstract
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 (ΔNp73).
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1 retracted
RETRACTED ARTICLE: p73α Regulation by Chk1 in Response to DNA Damage
González, S., Prives, C. L., & Cordon‐Cardo, C. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.22.8161-8171.2003 · Cited by 77
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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
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p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development
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Tumor spectrum analysis in p53-mutant mice
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p63 is a p53 homologue required for limb and epidermal morphogenesis
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Rescue of early embryonic lethality in mdm2-deficient mice by deletion of p53
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“p53 has an important developmental role in early mouse embryogenesis (E7-8d) as revealed when the autoregulatory feedback loop with MDM2 is removed and p53 levels remain uncontrolled (40, 41).”
Background
Cited by
Age-dependent DNA methylation of genes that are suppressed in stem cells is a hallmark of cancer
Teschendorff, A. E., Menon, U., Gentry-Maharaj, A., Ramus, S. J., Weisenberger, D. J., Shen, H., Campan, M., Noushmehr, H., Bell, C. G., Maxwell, A. P., et al. (2010) · Genome Research · doi:10.1101/gr.103606.109 · Cited by 855
The p53 family in differentiation and tumorigenesis
Stiewe, T. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2072 · Cited by 306
TAp63α induces apoptosis by activating signaling via death receptors and mitochondria
Gressner, O., Schilling, T., Lorenz, K., Schulze Schleithoff, E., Koch, A., Schulze‐Bergkamen, H., Maria Lena, A., Candi, E., Terrinoni, A., Valeria Catani, M., et al. (2005) · The EMBO Journal · doi:10.1038/sj.emboj.7600708 · Cited by 255
A planarian p53 homolog regulates proliferation and self-renewal in adult stem cell lineages
Pearson, B. J., & Alvarado, A. S. (2010) · Development · doi:10.1242/dev.044297 · Cited by 188
DNA repair and aging: The impact of the p53 family
Nicolai, S., Rossi, A., Di Daniele, N., Melino, G., Annicchiarico-Petruzzelli, M., & Raschellà, G. (2015) · Aging · doi:10.18632/aging.100858 · Cited by 118
Metadata
- Authors
- Moll, U. M., & Slade, N.
- Venue
- Molecular Cancer Research
- Published
- 2004-07-01
- Volume
- 2
- Issue
- 7
- Pages
- 371-386
- ISSN
- 1541-7786 (ISSN-L)
- 1557-3125
- OpenAlex
- W2313048860
- Cited by
- 486
- References
- 165
- FWCI
- 15.13
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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