ArticleOncogene2001
Increased p53 phosphorylation after microtubule disruption is mediated in a microtubule inhibitor- and cell-specific manner.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 67 citations in OpenAlex.
- Post-translational modifications of tubulin: their role in cancers and the regulation of signaling molecules.Cancer gene therapy · 2023Review
- Identification and characterization of SSE15206, a microtubule depolymerizing agent that overcomes multidrug resistance.Scientific reports · 2018Article
- The human papillomavirus E7 oncoprotein as a regulator of transcription.Virus research · 2017Review
- Orally active microtubule-targeting agent, MPT0B271, for the treatment of human non-small cell lung cancer, alone and in combination with erlotinib.Cell death & disease · 2014Article
- Synergistic action by multi-targeting compounds produces a potent compound combination for human NSCLC both in vitro and in vivo.Cell death & disease · 2014Article
- Prolonged mitotic arrest triggers partial activation of apoptosis, resulting in DNA damage and p53 induction.Molecular biology of the cell · 2012Article
- Bioinformatic analyses identifies novel protein-coding pharmacogenomic markers associated with paclitaxel sensitivity in NCI60 cancer cell lines.BMC medical genomics · 2011Article
- Mitotic slippage in non-cancer cells induced by a microtubule disruptor, disorazole C1.BMC chemical biology · 2010Article
- TTK/hMps1 mediates the p53-dependent postmitotic checkpoint by phosphorylating p53 at Thr18.Molecular and cellular biology · 2009Article
- Plk3 interacts with and specifically phosphorylates VRK1 in Ser342, a downstream target in a pathway that induces Golgi fragmentation.Molecular and cellular biology · 2009Article
- A novel triterpenoid isolated from the root bark of Ailanthus excelsa Roxb (Tree of Heaven), AECHL-1 as a potential anti-cancer agent.PloS one · 2009Article
- Cancer cells activate p53 in response to 10-formyltetrahydrofolate dehydrogenase expression.The Biochemical journal · 2005Article
- Article
- Silencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells.Molecular and cellular biology · 2003Article
- Paclitaxel increases p21 synthesis and accumulation of its AKT-phosphorylated form in the cytoplasm of cancer cells.Oncogene · 2003Article
- Enhanced microtubule-dependent trafficking and p53 nuclear accumulation by suppression of microtubule dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Protein kinase CK2 is involved in G2 arrest and apoptosis following spindle damage in epithelial cells.Oncogene · 2001Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
p53 is present at low levels in unstressed cells. Numerous cellular insults, including DNA damage and microtubule disruption, elevate p53 protein levels. Phosphorylation of p53 is proposed to be important for p53 stabilization and activation after genotoxic stress; however, p53 phosphorylation after microtubule disruption has not been analysed. The goal of the current study was to determine if p53 phosphorylation increases after microtubule disruption, and if so, to identify specific p53 residues necessary for microtubule inhibitor-induced phosphorylation. Two dimensional gel analyses demonstrated that the number of p53 phospho-forms in cells increased after treatment with microtubule inhibitors (MTIs) and that the pattern of p53 phosphorylation was distinct from that observed after DNA damage. p53 phosphorylation also varied in a MTI-dependent manner, as Taxol and Vincristine induced more p53 phospho-forms than nocodazole. Further, MTI treatment increased phosphorylation of p53 on serine-15 in epithelial tumor cells. In contrast, serine-15 phosphorylation of p53 did not increase in MTI-treated primary cultures of human fibroblasts. Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53. Taken together, the results of this study demonstrate that distinct p53 phospho-forms are induced by MTI treatment as compared to DNA damage and that p53 phosphorylation is mediated in a MTI- and cell-specific manner. Oncogene (2001) 20, 113 - 124.
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