Wip1 contributes to cell homeostasis maintained by the steady-state level of Wtp53
| العنوان: | Wip1 contributes to cell homeostasis maintained by the steady-state level of Wtp53 |
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| المؤلفون: | Sinto Sebastian, Guangzhi Dong, Hwan Ki Park, Fred Duafalia Dudimah, Peiwen Fei, Jayabal Panneerselvam, Jun Zhang |
| المصدر: | Cell Cycle. 10:2574-2582 |
| بيانات النشر: | Informa UK Limited, 2011. |
| سنة النشر: | 2011 |
| مصطلحات موضوعية: | Mitosis, Biology, Cell Line, Mice, Cell Cycle News & Views, chemistry.chemical_compound, Radiation, Ionizing, CDC2 Protein Kinase, Phosphoprotein Phosphatases, Animals, Humans, CHEK1, Phosphorylation, Molecular Biology, Mitotic catastrophe, Tissue homeostasis, Cyclin-dependent kinase 1, Wild type, Tyrosine phosphorylation, Cell Biology, G2-M DNA damage checkpoint, Cell biology, G2 Phase Cell Cycle Checkpoints, Protein Phosphatase 2C, chemistry, M Phase Cell Cycle Checkpoints, Tumor Suppressor Protein p53, Developmental Biology |
| الوصف: | 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. |
| تدمد: | 1551-4005 1538-4101 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::62dca963821410eacbe28fb34e1c0da7Test https://doi.org/10.4161/cc.10.15.15923Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....62dca963821410eacbe28fb34e1c0da7 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15514005 15384101 |
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