Cited by 595Cancer-related Molecular PathwaysUbiquitin and proteasome pathwaysCell death mechanisms and regulation

Divorcing ARF and p53: an unsettled case

Sherr, Charles J.·2006·Nature reviews. Cancer

Abstract

Mammalian cells that sustain oncogenic insults can invoke defensive programmes that either halt their division or trigger their apoptosis, but these countermeasures must be finely tuned to discriminate between physiological and potentially harmful growth-promoting states. By functioning specifically to oppose abnormally prolonged and sustained proliferative signals produced by activated oncogenes, the ARF tumour suppressor antagonizes functions of MDM2 to induce protective responses that depend on the p53 transcription factor and its many target genes. However, ARF has been reported to physically associate with proteins other than MDM2 and to have p53-independent activities, most of which remain controversial and poorly understood.

Integrity signals

Registry

Crossref · 10.1038/nrc1954

Cites

129 of 129 references verified0 citation errors · 0 not checkable

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  • Many tumors in mice and humans inactivate either p53 or ARF, which has led to the conclusion that the two proteins have an epistatic relationship.

    “Many tumors in mice and humans inactivate either p53 or ARF, leading to the conclusion that these two proteins have an epistatic relationship (Sherr, 2006).”

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Authors
Sherr, C. J.
Affiliations
St. Jude Children's Research Hospital (US)
Corresponding author
Sherr, Charles J.
Venue
Nature reviews. Cancer
Published
2006-08-17
Volume
6
Issue
9
Pages
663-673
ISSN
  • 1474-175X (ISSN-L)
  • 1474-1768
OpenAlex
W1989168159
Cited by
595
References
129
Citations by year
2026: 4 · 2025: 10 · 2024: 11 · 2023: 16 · 2022: 16 · 2021: 14 · 2020: 21 · 2019: 15 · 2018: 20 · 2017: 23 · 2016: 28 · 2015: 30 · 2014: 53 · 2013: 58 · 2012: 35
FWCI
4.86
Type
journal article
Language
en
Open access
closed
Locations
  • Nature reviews. Cancer (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
p53, MDM2, carcinogenesis, oncogene-induced senescence, apoptosis, ubiquitin ligase, tumor suppressor proteins
MeSH terms
Animals, Humans, Neoplasms, Signal Transduction, Tumor Suppressor Protein p53, Apoptosis, Tumor Suppressor Protein p14ARF, Proto-Oncogene Proteins c-mdm2

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