Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 416, Issue 1-2, Pages 33-46Publisher
SPRINGER
DOI: 10.1007/s11010-016-2693-2
Keywords
CDC25 phosphatase; Kinases; Cell cycle; Cancer; Intimal hyperplasia
Categories
Funding
- National Heart, Lung and Blood Institute, the National Institutes of Health, USA [R01 HL116042, R01 HL112597, R01 HL120659]
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Alterations in the cell-cycle regulatory genes result in uncontrolled cell proliferation leading to several disease conditions. Cyclin-dependent kinases (CDK) and their regulatory subunit, cyclins, are essential proteins in cell-cycle progression. The activity of CDK is regulated by a series of phosphorylation and dephosphorylation at different amino acid residues. Cell Division Cycle-25 (CDC25) plays an important role in transitions between cell-cycle phases by dephosphorylating and activating CDKs. CDC25B and CDC25C play a major role in G2/M progression, whereas CDC25A assists in G1/S transition. Different isomers of CDC25 expressions are upregulated in various clinicopathological situations. Overexpression of CDC25A deregulates G1/S and G2/M events, including the G2 checkpoint. CDC25B has oncogenic properties. Binding to the 14-3-3 proteins regulates the activity and localization of CDC25B. CDC25C is predominantly a nuclear protein in mammalian cells. At the G2/M transition, mitotic activation of CDC25C protein occurs by its dissociation from 14-3-3 proteins along with its phosphorylation at multiple sites within its N-terminal domain. In this article, we critically reviewed the biology of the activation/deactivation of CDC25 by kinases/phosphatases to maintain the level of CDK-cyclin activities and thus the genomic stability, clinical implications due to dysregulation of CDC25, and potential role of CDC25 inhibitors in diseases.
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