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Protein kinases in the control of mitosis : focus on nucleocytoplasmic trafficking

Gallant, P. and Fry, A. M. and Nigg, E. A.. (1995) Protein kinases in the control of mitosis : focus on nucleocytoplasmic trafficking. Journal of cell science. Supplement, 19. pp. 21-28.

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Official URL: http://edoc.unibas.ch/dok/A5249459

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Abstract

The eukaryotic cell nucleus is a highly dynamic organelle. This is illustrated most dramatically during mitosis, when the nuclear envelope breaks down, the nuclear lamina disassembles, chromosomes condense, and a microtubule-based spindle apparatus distributes sister chromatids to the dividing daughter cells. Many of these dramatic changes in nuclear architecture and microtubule organization are controlled by phosphorylation and dephosphorylation events. Whereas the cardinal role of cyclin-dependent kinases (CDKs) in the regulation of mitosis is well established, there is now clear evidence for the requirement of additional mitotic protein kinases. Studies into the regulation of CDKs and other mitotic kinases have revealed that these enzymes undergo cell cycle dependent changes in subcellular distribution, suggesting that localization may contribute to regulating their activities. This article describes some recent findings relating to the nucleocytoplasmic translocation of CDK/cyclin complexes at the onset of mitosis. In addition, it summarizes recent information on two novel human protein kinases which have been implicated in the control of mitotic progression.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum
05 Faculty of Science > Departement Biozentrum > Former Organization Units Biozentrum > Cell Biology (Nigg)
UniBasel Contributors:Nigg, Erich A.
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Note:Also published in: Organisation of the cell nucleus. - Cambridge : Company of Biologists. - S. 21-28 -- Publication type according to Uni Basel Research Database: Journal article
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Last Modified:02 Oct 2015 10:01
Deposited On:22 Mar 2012 13:59

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