ArticleOncogene2004
Control of cell cycle-dependent degradation of c-Ski proto-oncoprotein by Cdc34.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Systematic identification of CDC34 that functions to stabilize EGFR and promote lung carcinogenesis.EBioMedicine · 2020Article
- Structural insights into E1 recognition and the ubiquitin-conjugating activity of the E2 enzyme Cdc34.Nature communications · 2019Article
- Ski protein levels increase during in vitro progression of HPV16-immortalized human keratinocytes and in cervical cancer.Virology · 2013Article
- Intercellular variation in signaling through the TGF-β pathway and its relation to cell density and cell cycle phase.Molecular & cellular proteomics : MCP · 2012Article
- Regulation of the transforming growth factor β pathway by reversible ubiquitylation.Open biology · 2012Review
- Chromosomal instability in mouse embryonic fibroblasts null for the transcriptional co-repressor Ski.Journal of cellular physiology · 2012Article
- Identification of Ski as a target for Aurora A kinase.Biochemical and biophysical research communications · 2011Article
- Measuring the absolute abundance of the Smad transcription factors using quantitative immunoblotting.Methods in molecular biology (Clifton, N.J.) · 2010Article
- Transforming growth factor beta depletion is the primary determinant of Smad signaling kinetics.Molecular and cellular biology · 2009Article
- Ski and SnoN, potent negative regulators of TGF-beta signaling.Cell research · 2009Review
- To (TGF)beta or not to (TGF)beta: fine-tuning of Smad signaling via post-translational modifications.Cellular signalling · 2008Review
- Cdh1-anaphase-promoting complex targets Skp2 for destruction in transforming growth factor beta-induced growth inhibition.Molecular and cellular biology · 2007Article
- The Ski oncoprotein is upregulated and localized at the centrosomes and mitotic spindle during mitosis.Oncogene · 2005Article
- Factors of transforming growth factor beta signalling are co-regulated in human hepatocellular carcinoma.Virchows Archiv : an international journal of pathology · 2004Article
- Transcriptional cofactors Ski and SnoN are major regulators of the TGF-β/Smad signaling pathway in health and disease.Signal transduction and targeted therapyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
It is known that excess amounts of Ski, or any member of its proto-oncoprotein family, causes disruption of the transforming growth factor beta signal transduction pathway, thus causing oncogenic transformation of cells. Previous studies indicate that Ski is a relatively unstable protein whose expression levels can be regulated by ubiquitin-mediated proteolysis. Here, we investigate the mechanism by which the stability of Ski is regulated. We show that the steady-state levels of Ski protein are controlled post-translationally by cell cycle-dependent proteolysis, wherein Ski is degraded during the interphase of the cell cycle but is relatively stable during mitosis. Furthermore, we demonstrate that the ubiquitin-conjugating enzyme Cdc34 mediates cell cycle-dependent Ski degradation both in vitro and in vivo. Overexpression of dominant-negative Cdc34 stabilizes Ski and enhances its ability to antagonize TGF-beta signaling. Our data suggest that regulated proteolysis of Ski is one of the key mechanisms that control the threshold levels of this proto-oncoprotein, and thus prevents epithelial cells from becoming TGF-beta resistant.
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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.