ArticleMolecular and cellular biology2005
Transforming growth factor beta facilitates beta-TrCP-mediated degradation of Cdc25A in a Smad3-dependent manner.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed, 57 citations in OpenAlex.
- Improved recovery from skeletal muscle damage is largely unexplained by myofibrillar protein synthesis or inflammatory and regenerative gene expression pathways.American journal of physiology. Endocrinology and metabolism · 2021Trial
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication.Microorganisms · 2024Article
- Intricacies of TGF-β signaling in Treg and Th17 cell biology.Cellular & molecular immunology · 2023Review
- KAT6A Acetylation of SMAD3 Regulates Myeloid-Derived Suppressor Cell Recruitment, Metastasis, and Immunotherapy in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Effects of let-7c on the proliferation of ovarian carcinoma cells by targeted regulation of CDC25a gene expression.Oncology letters · 2018Article
- Radiotherapy induces cell cycle arrest and cell apoptosis in nasopharyngeal carcinoma via the ATM and Smad pathways.Cancer biology & therapy · 2017Article
- Article
- TGF-β Family Signaling in the Control of Cell Proliferation and Survival.Cold Spring Harbor perspectives in biology · 2017Review
- Article
- Posttranslational Regulation of Smads.Cold Spring Harbor perspectives in biology · 2016Review
- Identification of Four Mouse Diabetes Candidate Genes Altering β-Cell Proliferation.PLoS genetics · 2015Article
- The microRNA 424/503 cluster reduces CDC25A expression during cell cycle arrest imposed by transforming growth factor β in mammary epithelial cells.Molecular and cellular biology · 2014Article
- Expression of targeted ribozyme against telomerase RNA causes altered expression of several other genes in tumor cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- PD-1 inhibits T cell proliferation by upregulating p27 and p15 and suppressing Cdc25A.Cell cycle (Georgetown, Tex.) · 2012Article
- Selective effects of PD-1 on Akt and Ras pathways regulate molecular components of the cell cycle and inhibit T cell proliferation.Science signaling · 2012Article
- Absence of polo-like kinase 3 in mice stabilizes Cdc25A after DNA damage but is not sufficient to produce tumors.Mutation research · 2011Article
- Cdc25A regulates matrix metalloprotease 1 through Foxo1 and mediates metastasis of breast cancer cells.Molecular and cellular biology · 2011Article
- Regulation of EGFR protein stability by the HECT-type ubiquitin ligase SMURF2.Neoplasia (New York, N.Y.) · 2011Article
- A human cancer-predisposing polymorphism in Cdc25A is embryonic lethal in the mouse and promotes ASK-1 mediated apoptosis.Cell division · 2011Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Ubiquitin-dependent degradation of Cdc25A is a major mechanism for damage-induced S-phase checkpoint. Two ubiquitin ligases, the Skp1-cullin-beta-TrCP (SCFbeta-TrCP) complex and the anaphase-promoting complex (APCCdh1), are involved in Cdc25A degradation. Here we demonstrate that the transforming growth factor beta (TGF-beta)-Smad3 pathway promotes SCF(beta-TrCP)-mediated Cdc25A ubiquitination. Cells treated with TGF-beta, as well as cells transfected with Smad3 or a constitutively active type I TGF-beta receptor, exhibit increased ubiquitination and markedly shortened half-lives of Cdc25A. Furthermore, Cdc25A is stabilized in cells transfected with Smad3 small interfering RNA (siRNA) and cells from Smad3-null mice. TGF-beta-induced ubiquitination is associated with Cdc25A phosphorylation at the beta-TrCP docking site (DS82G motif) and physical association of Cdc25A with Smad3 and beta-TrCP. Cdc25A mutant proteins deficient in DS82G phosphorylation are resistant to TGF-beta-Smad3-induced degradation, whereas a Cdc25A mutant protein defective in APCCdh1 recognition undergoes efficient degradation. Smad3 siRNA inhibits beta-TrCP-Cdc25A interaction and Cdc25A degradation in response to TGF-beta. beta-TrCP2 siRNA also inhibits Smad3-induced Cdc25A degradation. In contrast, Cdh1 siRNA had no effect on Cdc25A down-regulation by Smad3. These data suggest that Smad3 plays a key role in the regulation of Cdc25A ubiquitination by SCFbeta-TrCP and that Cdc25A stabilization observed in various cancers could be associated with defects in the TGF-beta-Smad3 pathway.
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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.