ArticleCell cycle (Georgetown, Tex.)2010
Reactivating the ARF-p53 axis in AML cells by targeting ULF.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- TRIP12's role in the governance of DNA polymerase β involvement in DNA damage response and repair.Nucleic acids research · 2025Article
- The TRIP12 E3 ligase induces SWI/SNF component BRG1-β-catenin interaction to promote Wnt signaling.Nature communications · 2025Article
- E3 Ubiquitin LigaseCancers · 2023Article
- Helicobacter pylori pathogen inhibits cellular responses to oncogenic stress and apoptosis.PLoS pathogens · 2022Article
- E3 ubiquitin ligases in the acute leukemic signaling pathways.Frontiers in physiology · 2022Review
- The oncogenic E3 ligase TRIP12 suppresses epithelial-mesenchymal transition (EMT) and mesenchymal traits through ZEB1/2.Cell death discovery · 2021Article
- Proteasomal degradation of the tumour suppressor FBW7 requires branched ubiquitylation by TRIP12.Nature communications · 2021Article
- E3 Ubiquitin Ligase TRIP12: Regulation, Structure, and Physiopathological Functions.International journal of molecular sciences · 2020Review
- Landscape of Tumor Suppressor Mutations in Acute Myeloid Leukemia.Journal of clinical medicine · 2020Review
- The role of TP53 in acute myeloid leukemia: Challenges and opportunities.Genes, chromosomes & cancer · 2019Review
- Review
- GLTSCR2 promotes the nucleoplasmic translocation and subsequent degradation of nucleolar ARF.Oncotarget · 2017Article
- Article
- RNA-Seq analysis identifies aberrant RNA splicing of TRIP12 in acute myeloid leukemia patients at remission.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Review
- MYC cofactors: molecular switches controlling diverse biological outcomes.Cold Spring Harbor perspectives in medicine · 2014Review
- Differential effects on ARF stability by normal versus oncogenic levels of c-Myc expression.Molecular cell · 2013Article
- Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.Oncotarget · 2011Article
- Aberrant Expression of p14Tumor & microenvironmentArticle
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
The tumor suppressor ARF plays an essential role in the cellular response to oncogenic stress mainly through activation of p53. Nucleophosmin (NPM), a multifunctional protein, forms a stable protein complex with ARF in the nucleolus and protects ARF from the proteasome-mediated degradation. Notably, NPM is mutated in about one third of acute myeloid leukaemia (AML) patients and these mutations lead to aberrant cytoplasmic dislocation of nucleophosmin (NPM-c). Cytoplasmic NPM mutants lose their abilities to retain ARF in the nucleolus and fail to stabilize ARF. Thus, activation of the ARF-p53 axis is significantly compromised in these AML cells. We have recently identified the ubiquitin ligase of ARF (ULF) as a key factor that controls ARF turnover in human cells. Here, we found that the steady levels of both ARF and p53 are very low in human acute myeloid leukaemia OCI-AML3 cells expressing cytoplamsic dislocated nucleophosmin (NPM-c). As expected, ARF is very unstable and rapidly degraded by proteasome. Nevertheless, ULF knockdown stabilizes ARF and reactivates p53 responses in these AML cells. These results further demonstrate that ULF is a bona fide E3 ligase for ARF and also suggest that ULF is an important target for activating the ARF-p53 axis in human AML cells.
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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.