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(1/225) Nucleoplasmic calcium regulates cell proliferation through legumain.

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(2/225) Transcriptional regulation underlying recovery from a DNA damage-induced arrest.

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(3/225) RNA binding protein CUGBP2/CELF2 mediates curcumin-induced mitotic catastrophe of pancreatic cancer cells.

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(4/225) Cell cycle suspension: a novel process lurking in G(2) arrest.

Cell cycle checkpoint is a self-protective mechanism for cells to monitor genome integrity and ensure the high-fidelity transmission of genetic information to daughter cells. Insufficient function of cell cycle checkpoints has been demonstrated to partially account for tumor initiation, promotion and progression. In the ten melanoma cell lines that we tested in preliminary experiments, two human uveal melanoma cell lines, 92-1 and OCM-1, were found to be significantly different in terms of radiosensitivity but similar in DNA repair ability. Evident G 2 arrest was induced in both cell types and the maximum was reached at 16 h after irradiation regardless of X-rays or high-LET carbon beams. OCM-1 cells overrode the G 2 arrest and reentered the cell cycle right after reaching the maximum, whereas 92-1 could not. Upon 10 Gy of radiation, the cell cycle of 92-1 was suspended and remained unchanged for up to 5 d. The cell cycle suspension is a unique process lurking in G 2 arrest and related to cellular radiosensitivity. Its induction is dose-dependent and there is a dose threshold for it. The degradation of Cyclin B1 has been found related to the cell cycle suspension though, the mechanism of cell cycle suspension is still under investigation. Basing on our knowledge, this is the first report on cell cycle suspension and we present here a de novo mechanism to cellular radiosensitivity. Further clarification of the mechanism underlying cell cycle suspension is believed to be of significance in tumor radiosensitization or even direct tumor control.  (+info)

(5/225) Polycomb protein EZH2 regulates cancer cell fate decision in response to DNA damage.

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(6/225) Assessing 'radiosensitivity' with kinetic profiles of gamma-H2AX, 53BP1 and BRCA1 foci.

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(7/225) Wip1 contributes to cell homeostasis maintained by the steady-state level of Wtp53.

Wip1, a human protein Ser/Thr phosphatase also called PPM1D, stands for wild type p53 induced phosphatase 1. Emerging evidences indicate that Wip1 can act as an oncogene largely by turning off DNA damage checkpoint responses. Here we report an unrecognized role of Wipl in normally growing cells. Wip1 can be induced by wild type p53 under not only stressed but also non-stressed conditions. It can trigger G 2/M arrest in wild type p53 containing cells, which was attributed to the decreased Cdc2 kinase activity resulting at least partly from a high level of inhibitory tyrosine phosphorylation on Cdc2 protein at Tyr-15. Furthermore, we also found that Wip1 not only causes G 2/M arrest but also decreases cell death triggered by microtubule assembly inhibitor in mouse fibroblasts when wild type p53 function was restored. These results indicate that Wip1 can provide ample time for wild type p53-containing cells to prepare entry into mitosis and avoid encountering mitotic catastrophe. Therefore, Wipl may play important roles in cell/tissue homeostasis maintained by wild type p53 under normal conditions, enhancing our understanding of how p53 makes cell-fate decisions.  (+info)

(8/225) Role for hACF1 in the G2/M damage checkpoint.

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