p63 and p73, the ancestors of p53
Open accessAbstract
p73 and p63 are two homologs of the tumor suppressive transcription factor p53. Given the high degree of structural similarity shared by the p53 family members, p73 and p63 can bind and activate transcription from the majority of the p53-responsive promoters. Besides overlapping functions shared with p53 (i.e., induction of apoptosis in response to cellular stress), the existence of extensive structural variability within the family determines unique roles for p63 and p73. Their crucial and specific functions in controlling development and differentiation are well exemplified by the p63 and p73 knockout mouse phenotypes. Here, we describe the contribution of p63 and p73 to human pathology with emphasis on their roles in tumorigenesis and development.
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p73 is rarely mutated in cancers.
“in contrast, p73 is rarely mutated in cancers (14, 16).”
From Potentiation of carboplatin-mediated DNA damage by the Mdm2 modulator Nutlin-3a in a humanized orthotopic breast-to-lung metastatic model (2015) · cites this paper as [16]
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- Authors
- Dotsch, V., Bernassola, F., Coutandin, D., Candi, E., & Melino, G.
- Affiliations
- University of Rome Tor Vergata (IT)
- Goethe University Frankfurt (DE)
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2010-05-19
- Volume
- 2
- Issue
- 9
- Pages
- a004887-a004887
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC2926756
- OpenAlex
- W2135458195
- Cited by
- 326
- References
- 80
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 16 · 2023: 23 · 2022: 14 · 2021: 27 · 2020: 15 · 2019: 21 · 2018: 23 · 2017: 18 · 2016: 25 · 2015: 26 · 2014: 20 · 2013: 25 · 2012: 32
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- p63, p73, p53 family, apoptosis, carcinogenesis, developmental regulation, human disease, transcriptional activation
- MeSH terms
- Tumor Protein p73, Animals, DNA-Binding Proteins, Humans, Nuclear Proteins, Transcription Factors, Trans-Activators, Tumor Suppressor Protein p53, Evolution, Molecular, Protein Isoforms, Tumor Suppressor Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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