ArticleMolecular biology reports2010
Plk1 phosphorylation of Topors is involved in its degradation.
Article in Molecular biology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- The status of p53 affects the efficacy of PLK1 inhibitor BI6727 in prostate cancer cells.Frontiers in cell and developmental biology · 2025Article
- Review
- Plk1 Inhibitors in Cancer Therapy: From Laboratory to Clinics.Molecular cancer therapeutics · 2016Review
- Jade-1S phosphorylation induced by CK1α contributes to cell cycle progression.Cell cycle (Georgetown, Tex.) · 2016Article
- Plk1-mediated phosphorylation of UAP56 regulates the stability of UAP56.Molecular biology reports · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Topors is a DNA topoisomerase I- and p53-binding protein, and mainly functions as a p53 regulator. Accumulating evidence also supports the notion that Topors plays the role as a negative regulator of cell growth, and possibly as a tumor suppressor. Here, we demonstrated that Topors is also involved in normal mitotic progression, since Topors depletion delays mitotic entry and affects mitotic progression. Furthermore, Topors is degradated in response to the activation of the spindle checkpoint. Significantly, Polo-like kinase 1 (Plk1)-associated phosphorylation of Topors at S718 is essential for nocodazole-induced degradation of Topors.
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Registered trials
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