ArticleOncogene2000
Cdc25A stability is controlled by the ubiquitin-proteasome pathway during cell cycle progression and terminal differentiation.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 70 citations in OpenAlex.
- Identification of VWA5A as a novel biomarker for inhibiting metastasis in breast cancer by machine-learning based protein prioritization.Scientific reports · 2024Article
- mInternational journal of biological sciences · 2024Article
- Proteomic Assessment of Extracellular Vesicles from Canine Tissue Explants as a Pipeline to Identify Molecular Targets in Osteosarcoma: PSMD14/Rpn11 as a Proof of Principle.International journal of molecular sciences · 2022Article
- Theranostic Interpolation of Genomic Instability in Breast Cancer.International journal of molecular sciences · 2022Review
- Ubiquitin-Specific Protease 29 Regulates Cdc25A-Mediated Tumorigenesis.International journal of molecular sciences · 2021Article
- The REGγ inhibitor NIP30 increases sensitivity to chemotherapy in p53-deficient tumor cells.Nature communications · 2020Article
- A population of G2-arrested cells are selected as sensory organ precursors for the interommatidial bristles of the Drosophila eye.Developmental biology · 2017Article
- Acetylation and deacetylation of Cdc25A constitutes a novel mechanism for modulating Cdc25A functions with implications for cancer.Oncotarget · 2016Article
- David and Goliath: chemical perturbation of eukaryotes by bacteria.Journal of industrial microbiology & biotechnology · 2016Review
- Role and regulation of Cdc25A phosphatase in neuron death induced by NGF deprivation orCell death discovery · 2016Article
- Checkpoint kinase1 (CHK1) is an important biomarker in breast cancer having a role in chemotherapy response.British journal of cancer · 2015Article
- Voltage sensitive phosphatases: emerging kinship to protein tyrosine phosphatases from structure-function research.Frontiers in pharmacology · 2015Review
- Acrolein- and 4-Aminobiphenyl-DNA adducts in human bladder mucosa and tumor tissue and their mutagenicity in human urothelial cells.Oncotarget · 2014Article
- Article
- CRL Ubiquitin Ligases and DNA Damage Response.Frontiers in oncology · 2012Article
- Absence of polo-like kinase 3 in mice stabilizes Cdc25A after DNA damage but is not sufficient to produce tumors.Mutation research · 2011Article
- JAZ mediates G1 cell cycle arrest by interacting with and inhibiting E2F1.Cell cycle (Georgetown, Tex.) · 2011Article
- A human cancer-predisposing polymorphism in Cdc25A is embryonic lethal in the mouse and promotes ASK-1 mediated apoptosis.Cell division · 2011Article
- Article
- Id1 enhances RING1b E3 ubiquitin ligase activity through the Mel-18/Bmi-1 polycomb group complex.Oncogene · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Members of the cdc25 family are protein phosphatases that play pivotal roles in cell cycle progression. Cdc25A has been shown to be a critical regulator of the G1/S transition of mammalian cells and to be a myc-target gene with oncongenic properties. We investigated the regulation of cdc25A during terminal differentiation using myeloblastic leukemia M1 cells, that can be induced to undergo differentiation into macrophages by interleukin-6 (IL-6) treatment. In this report it is shown that cdc25A protein is degraded by the ubiquitin-proteasome machinery in both terminally differentiating and cycling cells. Cdc25A was found to have two major peaks of accumulation during cell cycle progression, one in G1 and the other in S/G2. Evidence was obtained that degradation of cdc25A by the ubiquitin-proteasome machinery in terminally differentiating myeloid cells is accelerated compared to cycling cells. Moreover, deregulated expression of c-myc in M1 cells, which had been previously shown to block terminal differentiation, was also found to block IL-6 induced degradation of cdc25A.
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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.