Polo-like Kinase

Supporting information

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.

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Gene Species Gene Symbol Gene Accession No. Protein Accession No.
PLK1 Human PLK1 NM_005030 P53350
Mouse Plk1 NM_011121 Q07832
Rat Plk1 NM_017100 Q62673
PLK2 Human PLK2 NM_006622 Q9NYY3
Mouse Plk2 NM_152804 P53351
Rat Plk2 NM_031821 Q9R012
View all Polo-like Kinase Gene Data »

Literature for Polo-like Kinase

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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.

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Checkpoint Kinases & the DNA Damage Response

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Cell Cycle Kinases Poster

A summary of the response of the checkpoint kinase signaling network to DNA damage, including activation of DNA repair, cell-cycle arrest, senescence and apoptosis.

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