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The focus of this pathway is to illustrate the role of Polo-like Kinase 3 (Plk3 also known as Prk and Fnk) as part of the regulatory cascade leading to apoptosis and the arrest cell cycle progression prior to M phase. Phosphorylation of Cdc25C on serine-216 causes the arrest of the cell cycle at the G2/M phase border by preventing Cdc25C from activating cyclinB1/Cdk1. Xie et al. demonstrated that Plk3, like Chk1 and Chk2, also phosphorylates Cdc25C on serine-216 contributing to cell cycle arrest. Additionally they found that Plk3 also phosphorylates p53 on serine 20, a step that is stimulatory in the process leading up to p53-mediated apoptosis. Wang Q et al. found that Plk3 is closely associated with the centrosome and that this is dependent on the integrity of the microtubules. Expression of constitutively active or defective Plk3 kinase had significant defects on the shape and nature of the microtubule apparatus of the cell. In either case cell cycle progression was halted and apoptosis occurred. (This definition may be outdated - see the DesignNote.)
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