ArticleProceedings of the National Academy of Sciences of the United States of America2005
Beta-TrCP recognizes a previously undescribed nonphosphorylated destruction motif in Cdc25A and Cdc25B phosphatases.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 124 citations in OpenAlex.
- TFEB degradation is regulated by an IKK/β-TrCP2 phosphorylation-ubiquitination cascade.Nature communications · 2026Article
- Oncogenic and immunological roles of LAMP5 across cancers and its potential utility in bladder cancer.Apoptosis : an international journal on programmed cell death · 2026Article
- Novel function of GTPBP2 in promoting hepatocellular carcinoma progression through inhibition of BTRC-mediated KRAS degradation.Cancer cell international · 2026Article
- The timing of maternal protein degradation during mammalian preimplantation development is species-specific.Reproduction (Cambridge, England) · 2025Article
- SKP1-CUL1-F-box: Key molecular targets affecting disease progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Ubiquitination Enzymes in Cancer, Cancer Immune Evasion, and Potential Therapeutic Opportunities.Cells · 2025Review
- Exosomes derived from hUC-MSCs exhibit ameliorative efficacy upon previous cesarean scar defect via orchestrating β-TrCP/CHK1 axis.Scientific reports · 2025Article
- Proteomic analysis reveals a PLK1-dependent G2/M degradation program and a role for AKAP2 in coordinating the mitotic cytoskeleton.Cell reports · 2024Article
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- Novel targets of β-TrCP cooperatively accelerate carbohydrate and fatty acid consumption.Journal of cellular physiology · 2024Article
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- Review
- Cyclin A-CDK1 suppresses the expression of the CDK1 activator CDC25A to safeguard timely mitotic entry.The Journal of biological chemistry · 2023Article
- Extracellular matrix stiffness regulates degradation of MST2 via SCFBiochimica et biophysica acta. General subjects · 2022Article
- Revealing β-TrCP activity dynamics in live cells with a genetically encoded biosensor.Nature communications · 2022Article
- Regulated interaction of ID2 with the anaphase-promoting complex links progression through mitosis with reactivation of cell-type-specific transcription.Nature communications · 2022Article
- Regulation of Epithelial-Mesenchymal Plasticity by the E3 Ubiquitin-Ligases in Cancer.Cancers · 2020Review
- Regulation of cell cycle drivers by Cullin-RING ubiquitin ligases.Experimental & molecular medicine · 2020Review
- The neglected part of early embryonic development: maternal protein degradation.Cellular and molecular life sciences : CMLS · 2020Review
- F-Box Proteins and Cancer.Cancers · 2020Review
12 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beta-TrCP, the F-box protein of the SCF(beta-TrCP) ubiquitin ligase (SCF, Skp1/Cul1/F-box protein), recognizes the doubly phosphorylated DSG motif (DpSGPhiXpS) in various SCF(beta-TrCP) target proteins. The Cdc25A phosphatase, a key cell-cycle regulator in vertebrate cells, undergoes a rapid ubiquitin-dependent degradation in response to genotoxic stress. Beta-TrCP binds to the DSG motif of human Cdc25A in a manner dependent on Chk1 and other unknown kinases. However, Xenopus Cdc25A does not have a DSG motif at the corresponding site of human Cdc25A. Here, we report that both Xenopus Cdc25A and human Cdc25A have a previously undescribed nonphosphorylated DDG motif (DDGPhiXD) for recognition by beta-TrCP. When analyzed by using Xenopus eggs, the binding of beta-TrCP to the DDG motif is essential for the Chk1-induced ubiquitination and degradation of Xenopus Cdc25A and also plays a role in the degradation of human Cdc25A. The DDG motif also exists in human Cdc25B phosphatase (another key cell-cycle regulator), binds beta-TrCP strongly, and is essential for the ubiquitination and degradation of the (labile) phosphatase in normal conditions. We provide strong evidence that, in both Cdc25A and Cdc25B, the binding (efficiency) of beta-TrCP to the DDG motif is regulated by nearby residues, while ubiquitination is regulated by other events in addition to the beta-TrCP binding. Finally, our additional data suggest that beta-TrCP may recognize nonphosphorylated DDG-like motifs in many other proteins, including X11L (a putative suppressor of beta-amyloid production) and hnRNP-U (a pseudosubstrate of SCF(beta-TrCP)).
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