Cited by 103Cancer-related Molecular PathwaysDNA Repair MechanismsCell death mechanisms and regulation

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Differential requirement for p19ARF in the p53-dependent arrest induced by DNA damage, microtubule disruption, and ribonucleotide depletion

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Khan, Shireen Hussain, Moritsugu, Janet, Wahl, Geoffrey M.·2000·Proceedings of the National Academy of Sciences

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Abstract

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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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
DOI: 10.1073/pnas.97.7.3266
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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Differential requirement for p19ARF in the p53-dependent arrest induced by DNA damage, microtubule disruption, and ribonucleotide depletion

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