Polo-like kinases (PLKs) are a family of four serine/threonine protein kinases that are critical regulators of cell cycle progression, mitosis, cytokinesis, and the DNA damage response. PLK1, -2 and -3 are ubiquitously expressed, whereas PLK4 is restricted to a few tissues including the testes and the thymus.
The mRNA and protein expression of PLK1, -2 and -4 are coordinately regulated during cell cycle progression, but PLK3 levels are independent of the other three family members. Furthermore, PLK3 is a much more stable protein than PLK1, -2 or -4. PLK1 is the most well characterized member of this family and strongly promotes the progression of cells through mitosis. During the various stages of mitosis PLK1 localizes to the centrosomes, kinetochores and central spindle.
PLKs are dysregulated in a variety of human cancers. PLK1 overexpression correlates with cellular proliferation and poor prognosis. PLK2 and PLK3 are involved in checkpoint-mediated cell cycle arrest to ensure genetic stability. Loss-of-function mutations in these enzymes can lead to oncogenic transformation.View all products for Polo-like Kinase »
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Literature for Polo-like Kinase
Cancer Research Guide
A collection of over 350 products for cancer research, the guide contains modulators of:
- Receptor Signaling
- Cell Cycle and DNA Damage Repair
- Cell Death and Drug Resistance
- Invasion and Metastasis
Kinase Product Listing
A collection of over 350 products for kinase research, the listing includes inhibitors of:
- Receptor Tyrosine Kinases
- Protein Kinases A, C, G and D
- PI-3 Kinase, Akt and mTOR
- Receptor Serine/Threonine Kinases
Cell Cycle Kinases Poster
Written by Michelle D. Garrett and Ian Collins, this poster summarizes the response of the checkpoint kinase signaling network to DNA damage, including activation of DNA repair, cell-cycle arrest, senescence and apoptosis. It also highlights the different types of DNA damage that can occur and some of the treatment methods that are utilized in cancer. Compounds available from Tocris are listed.Request copy | View all posters
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