ArticleMolecular cell2013
Differential effects on ARF stability by normal versus oncogenic levels of c-Myc expression.
Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 54 citations in OpenAlex.
- TP53-mutated myelodysplastic syndromes and acute myeloid leukemia: a comprehensive overview of targeted approaches.Frontiers in oncology · 2026Review
- Antimicrobial and Anticancer Activities ofNutrients · 2025Article
- SUMOylation of the lysine-less tumor suppressor p14ARF counters ubiquitylation-dependent degradation.Cell death & disease · 2025Article
- The Role of a Novel TRIP12 Mutation in Intellectual Disability: A Molecular and Clinical Investigation in Multiplex Family.Journal of molecular neuroscience : MN · 2025Article
- Oral intake of Hibiscus sabdariffa L. increased c-Myc and caspase-3 gene expression and altered microbial population in colon of BALB/c mice induced to preneoplastic lesions.European journal of nutrition · 2025Article
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Article
- Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies.MedComm · 2023Review
- TP53 Alterations in Myelodysplastic Syndromes and Acute Myeloid Leukemia.Biomedicines · 2023Review
- Helicobacter pylori pathogen inhibits cellular responses to oncogenic stress and apoptosis.PLoS pathogens · 2022Article
- PRMT1 promotes the tumor suppressor function of p14The EMBO journal · 2021Article
- Tumor-associated antigen Prame targets tumor suppressor p14/ARF for degradation as the receptor protein of CRL2Cell death and differentiation · 2021Article
- The oncogenic E3 ligase TRIP12 suppresses epithelial-mesenchymal transition (EMT) and mesenchymal traits through ZEB1/2.Cell death discovery · 2021Article
- E3 Ubiquitin Ligase TRIP12: Regulation, Structure, and Physiopathological Functions.International journal of molecular sciences · 2020Review
- Post-Translational Regulation of ARF: Perspective in Cancer.Biomolecules · 2020Review
- The E3 ubiquitin ligase TRIP12 participates in cell cycle progression and chromosome stability.Scientific reports · 2020Article
- The nucleolus: a central response hub for the stressors that drive cancer progression.Cellular and molecular life sciences : CMLS · 2019Review
- Long non-coding RNA PVT1 interacts with MYC and its downstream molecules to synergistically promote tumorigenesis.Cellular and molecular life sciences : CMLS · 2019Review
- Review
- The nucleolus, an ally, and an enemy of cancer cells.Histochemistry and cell biology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
ARF suppresses aberrant cell growth upon c-Myc overexpression by activating p53 responses. Nevertheless, the precise mechanism by which ARF specifically restrains the oncogenic potential of c-Myc without affecting its normal physiological function is not well understood. Here, we show that low levels of c-Myc expression stimulate cell proliferation, whereas high levels inhibit by activating the ARF/p53 response. Although the mRNA levels of ARF are induced in both scenarios, the accumulation of ARF protein occurs only when ULF-mediated degradation of ARF is inhibited by c-Myc overexpression. Moreover, the levels of ARF are reduced through ULF-mediated ubiquitination upon DNA damage. Blocking ARF degradation by c-Myc overexpression dramatically stimulates the apoptotic responses. Our study reveals that ARF stability control is crucial for differentiating normal (low) versus oncogenic (high) levels of c-Myc expression and suggests that differential effects on ULF- mediated ARF ubiquitination by c-Myc levels act as a barrier in oncogene-induced stress responses.
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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.