ArticleNature2010
Transcription-independent ARF regulation in oncogenic stress-mediated p53 responses.
Article in Nature, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 101 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
101 citing papers in PubMed, 162 citations in OpenAlex.
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- The role of HECT-type E3 ubiquitin ligases in DNA damage response and repair.Cell death discovery · 2025Review
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- SUMOylation of the lysine-less tumor suppressor p14ARF counters ubiquitylation-dependent degradation.Cell death & disease · 2025Article
- TRIP12's role in the governance of DNA polymerase β involvement in DNA damage response and repair.Nucleic acids research · 2025Article
- Helicobacter pylori activates DOPEY1 to promote p53 degradation through the USP7/TRIP12 axis in gastric tumorigenesis.Oncogene · 2025Article
- Genome-wide screening in human embryonic stem cells identifies genes and pathways involved in the p53 pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- A ligand discovery toolbox for the WWE domain family of human E3 ligases.Communications biology · 2024Article
- Elongin B promotes breast cancer progression by ubiquitinating tumor suppressor p14/ARF.Cell biology and toxicology · 2024Article
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- TATDN2 resolution of R-loops is required for survival of BRCA1-mutant cancer cells.Nucleic acids research · 2023Article
- Control of TGFβ signalling by ubiquitination independent function of E3 ubiquitin ligase TRIP12.Cell death & disease · 2023Article
- CRISPR/Cas9-mediated knockout of the ubiquitin variant UbKEKS reveals a role in regulating nucleolar structures and composition.Biology open · 2023Article
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- CRL2Oncogene · 2022Article
- An Update to Hallmarks of Cancer.Cureus · 2022Review
- E3 ubiquitin ligases in the acute leukemic signaling pathways.Frontiers in physiology · 2022Review
- TRIP12 ubiquitination of glucocerebrosidase contributes to neurodegeneration in Parkinson's disease.Neuron · 2021Article
- Fused in sarcoma regulates DNA replication timing and kinetics.The Journal of biological chemistry · 2021Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The tumour suppressor ARF is specifically required for p53 activation under oncogenic stress. Recent studies showed that p53 activation mediated by ARF, but not that induced by DNA damage, acts as a major protection against tumorigenesis in vivo under certain biological settings, suggesting that the ARF-p53 axis has more fundamental functions in tumour suppression than originally thought. Because ARF is a very stable protein in most human cell lines, it has been widely assumed that ARF induction is mediated mainly at the transcriptional level and that activation of the ARF-p53 pathway by oncogenes is a much slower and largely irreversible process by comparison with p53 activation after DNA damage. Here we report that ARF is very unstable in normal human cells but that its degradation is inhibited in cancerous cells. Through biochemical purification, we identified a specific ubiquitin ligase for ARF and named it ULF. ULF interacts with ARF both in vitro and in vivo and promotes the lysine-independent ubiquitylation and degradation of ARF. ULF knockdown stabilizes ARF in normal human cells, triggering ARF-dependent, p53-mediated growth arrest. Moreover, nucleophosmin (NPM) and c-Myc, both of which are commonly overexpressed in cancer cells, are capable of abrogating ULF-mediated ARF ubiquitylation through distinct mechanisms, and thereby promote ARF stabilization in cancer cells. These findings reveal the dynamic feature of the ARF-p53 pathway and suggest that transcription-independent mechanisms are critically involved in ARF regulation during responses to oncogenic stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.