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1. |
ectopic expression of PFKFB3 increased the expression of several key cell cycle proteins, including cyclin-dependent kinase (Cdk)-1, Cdc25C, and cyclin D3 and decreased the expression of the cell cycle inhibitor p27 |
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2. |
Cdc25C has a role in sensitivity of tumor cells to doxorubicin-induced cell death |
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3. |
Downregulation of the phosphatase CDC25A could solely be responsible for the slow growth phenotype in MCF10A/Bcl-2 cells. |
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4. |
study reports that a fraction of Cdc25C localises to centrosomes in a cell cycle-dependent fashion, as of late S phase and throughout G2 and mitosis; data suggest an unexpected function for Cdc25C at the G2/M transition, in dephosphorylation of Cdk1 |
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5. |
Observational study of gene-disease association. (HuGE Navigator) |
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6. |
The expression of CDC25A, CDC25B and the proliferation marker Ki-67 are not associated with prognosis in LSCC |
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7. |
Five novel splicing isoforms were detected, and the splicing patterns were generally distinct in neoplastic samples compared with healthy controls. |
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8. |
Cdc25C is a dual specificity phosphatase essential for dephosphorylation and activation of cyclin-dependent kinase is a prerequisite step for mitosis in all eucaryotes. Cdc25C activation requires phosphorylation. |
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9. |
cdc25C phosphatase plays a role in viral replication and that this role extends beyond its function of activating cdc2 for initiation of the ICP22-dependent cascade for upregulation of gamma(2) gene expression. |
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10. |
both U(L)13 and U(S)3 viral kinases phosphorylate cdc25C and ICP22; however, in infected cells, the ability of cdc25C to activate cdc2 by dephosphorylation of the inactive cdc2 protein is reduced |
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11. |
First-time evidence was provided for the existence of multiple species of Cdc25C in mitotic cell extracts. |
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12. |
PP2A:B56delta as a key upstream regulator of Cdk1 activity upon exit from mitosis |
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13. |
p53 like other binding partners of cdc25C, regulates entry into mitosis by binding to cdc25C |
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14. |
Cdc25B, but not Cdc25C, is capable of inhibiting cellular proliferation in a manner dependent upon its catalytic activity |
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15. |
Cdc25C is located in the cytoplasm at defined dense structures, which according to immunofluorescence analysis, electron microscopy as well as biochemical subfractionation, are proven to be the centrosomes. |
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16. |
binding to VPR protein in human cell lines correlates with G2 arrest |
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17. |
DNA damage-induced down-regulation of human Cdc25C |
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18. |
In Lzts1(-/-) mouse embryo fibroblasts (MEFs), Cdc25C degradation was increased during M phase, resulting in decreased Cdk1 activity. |
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19. |
cdc25C is located in the cytoplasm at defined dense structures which by immunofluorescence analysis as well as by biochemical subfractionation turned out to be the Golgi apparatus. |
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20. |
results suggest that Plk1 phosphorylates Cdc25C on Ser198 and regulates nuclear translocation of Cdc25C during prophase |
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21. |
role of degradation by oxidative stress in induction of cell cycle arrest |
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22. |
phosphorylation by Chk2 |
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23. |
Vpr promotes cell cycle arrest at the G(2)/M phase by facilitating association of 14-3-3 and Cdc25C |
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24. |
Partial or complete loss of Lzts1 downregulates Cdc25C and inhibits Cdk1 activity during mitosis, leading to premature transition from metaphase to anaphase. |
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25. |
Ca2+ promotes erythrocyte band 3 tyrosine phosphorylation via dissociation of phosphotyrosine phosphatase from band 3. |
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26. |
These results demonstrate that the MAPK ERK signaling pathway contributes to the p53-independent antiproliferative functions of p14ARF. Furthermore, they identify a new mechanism by which phosphorylation at serine 216 participates to Cdc25C inactivation. |
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27. |
Crystallization experiments of PLK1 protein in complex with an unphosphorylated and a phosphorylated target peptide from Cdc25C yield crystals suitable for X-ray diffraction analysis. |
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28. |
Vitamin C transiently arrests cancer cell cycle progression in S phase and G2/M boundary by modulating the kinetics of activation of CDC25C. |
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29. |
Data suggests that CDC25C might play an important role in prostate cancer progression and could be used to monitor and predict the aggressiveness of this disease. |
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30. |
cdc25C not only plays a role at the G2/M transition but also in the modulation of DNA replication |
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31. |
Analysis of cell cycle profile and cell cycle regulatory proteins indicated that arsenite arrested cell cycle at G(2)/M phase, partially through induction of cell division cycle 25 (Cdc25) isoform C (Cdc25C) degradation via ubiquitin-proteasome pathways |
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32. |
CDC25C translocation to the cell nucleus upon entry into mitosis is coordinated by Plk3 |
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33. |
Data suggest that Pim-1 activates Cdc25C by a direct phosphorylation and can thereby assume the function of a positive cell cycle regulator at the G2/M transition. |
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34. |
Chk1-mediated phosphorylation of Cdc25C plays a major role in response to LOR-mediated G(2)/M arrest. Although the Chk1-mediated cell growth arrest in a tumor cell line. |
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35. |
Phosphorylation of cdc25c can be used to test whether a pharmacologic inhibitor of Plk1 would exert the same cellular effects as interference with Plk1 on an mRNA level. |
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36. |
In A2780 cells, ERK1/2 interacts with Cdc25C in interphase and phosphorylates Cdc25C in mitosis. Inhibition of ERK activation partially inhibits T48 phosphorylation, Cdc25C activation, and mitotic induction. |
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37. |
downregulation of Cdc25C is mediated by p53 via two independent mechanisms, one involving direct binding to the cdc25C promoter |
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38. |
Human CDC25B and CDC25C differ by their ability to restore a functional checkpoint response after gene replacement in fission yeast |
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39. |
CDC25C is phosphorylated on Ser 214 during mitosis which, in turn, prevents phosphorylation of Ser 216. HeLa cells depeleted of endogenous CDC25C, when treated with exogenous CDC25C, had a substantial delay to mitotic entry. |