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Dual role of CDK1 in tumorigenesis and chemotherapeutic sensitivity.

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posted on 24.08.2011 by Chunyu Zhang, Abdel G. Elkahloun, Matthew Robertson, Joell J. Gills, Junji Tsurutani, Joanna H. Shih, Junya Fukuoka, M. Christine Hollander, Curtis C. Harris, William D. Travis, Jin Jen, Phillip A. Dennis

A. A model of CDK1 activation. When inactive p-Y15/T14 CDK1 is dephosphorylated on Y15 and T14 by CDC25A, it associates with Cyclin A/B and becomes active within the cytoplasm, then quickly translocates into the nucleus, where it promotes G1 to S and G2/M transitions. Active CDK1 is inactivated via sequential phosphorylation of Y15 and T14 by Wee1 and Myt1, and sequestrated by 14-3-3σ in the cytoplasm. This process repeats with cell cycling to drive cellular proliferation. B. A diagram to illustrate the dual role of CDK1 as a tumorigenic driver in lung carcinogenesis and a sensitizer in chemotherapeutic responsiveness.

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