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High affinity and selective PLK4 inhibitor (Ki = 0.16 nM). Exhibits >1000-fold selectivity for PLK4 over Aurora A and Aurora B. Depletes centriole and centrosome levels in vitro. Induces cell cycle arrest in normal human cell lines in a p53-dependent manner.
Sold with the permission of the Ludwig Institute for Cancer Research Ltd
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 633.65. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.58 mL||7.89 mL||15.78 mL|
|5 mM||0.32 mL||1.58 mL||3.16 mL|
|10 mM||0.16 mL||0.79 mL||1.58 mL|
|50 mM||0.03 mL||0.16 mL||0.32 mL|
References are publications that support the biological activity of the product.
Wong et al (2015) Reversible centriole depletion with an inhibitor of Polo-like kinase 4. Science 348 1155 PMID: 25931445
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Keywords: Centrinone, Centrinone supplier, High, affinity, selective, PLK4, inhibitors, inhibits, centriole, centrosome, Polo-like, Kinase, Mitosis, 5687, Tocris Bioscience
Citations for Centrinone
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Reviews for Centrinone
Average Rating: 4 (Based on 1 Review.)
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I have used this product in HeLa cells to abolish centrosomes and then track the recruitment kinetics of centriole biogenesis
Literature in this Area
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Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.