The DOI matches its Crossref record; 59 of the 61 references it cites were found in a registry or an index.
Differential requirement for p19ARF in the p53-dependent arrest induced by DNA damage, microtubule disruption, and ribonucleotide depletion
Open accessAbstract
p19ARF has been implicated as a key regulator of p53 stability and activation. While numerous stresses activate the p53 growth arrest pathway, those requiring p19ARF remain to be elucidated. We used p19ARF knockout mouse embryo fibroblasts to show that DNA damage and microtubule disruption require p19ARF to induce p53 responses, whereas ribonucleotide depletion and inhibition of RNA synthesis by low doses of actinomycin D do not. The data provide evidence that the arrest pathway activated by ribonucleotide depletion involves some different signal transducers than those activated by DNA damage or microtubule disruption. We also present biochemical analyses that provide insights into the mechanism by which p53 and p19ARF cooperate in normal cells to induce cell cycle arrest.
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“p19 Arf is not required for p53 induction by 𝛄 irradiation in vivo (25), although these observations appear to be at odds with its requirement in sustained cell cycle arrest after DNA damage in vitro (26).”
From Ink4a / Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouse (2007) · cites this paper as [26]
In the citing paper
“p19 Arf and, to a lesser extent, p16 Ink4a have been shown to play a role in the activation of cellular senescence and immortalization on passaging of primary mouse cells in culture (26, 43, 44).”
From Ink4a / Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouse (2007) · cites this paper as [26]
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Cited by
Sorted by citations
The RB and p53 pathways in cancer
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Metadata
- Authors
- Khan, S. H., Moritsugu, J., & Wahl, G. M.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Wahl, Geoffrey M.
- ORCID
- Wahl, Geoffrey M.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2000-03-14
- Volume
- 97
- Issue
- 7
- Pages
- 3266-3271
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC16227
- OpenAlex
- W2090930894
- Cited by
- 103
- References
- 61
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 1 · 2021: 1 · 2018: 1 · 2017: 3 · 2016: 2 · 2015: 2 · 2014: 3 · 2013: 9 · 2012: 3
- FWCI
- 5.74
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (CA61449, R01CA061449, 1T32CA64041, T32CA064041)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p19ARF, p53, cell cycle arrest, DNA damage response, microtubule disruption, actinomycin D, p53 stabilization, p53 activation, signal transduction, p16INK4a
- MeSH terms
- Animals, Cells, Cultured, DNA Damage, Microtubules, Polyploidy, Proteins, Ribonucleotides, Blotting, Western, Nocodazole, Tumor Suppressor Protein p53, Mice, Knockout, Tumor Suppressor Protein p14ARF, Mice
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