| Inhibitory phosphorylation of cyclin-dependent kinase 1 as a compensatory mechanism for mitosis exit. | |
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MedLine Citation:
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PMID: 21262764 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The current paradigm states that exit from mitosis is triggered by the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) acting in concert with an activator called CDC20. While this has been well established for a number of systems, the evidence of a critical role of CDC20 in somatic cells is not unequivocal. In this study, we reexamined whether mitotic exit can occur properly after CDC20 is depleted. Using single-cell analysis, we found that CDC20 depletion with small interfering RNAs (siRNAs) significantly impaired the degradation of APC/C substrates and delayed mitotic exit in various cancer cell lines. The recruitment of cyclin B1 to the core APC/C was defective after CDC20 downregulation. Nevertheless, CDC20-depleted cells were still able to complete mitosis, albeit requiring twice the normal time. Intriguingly, a high level of cyclin-dependent kinase 1 (CDK1)-inhibitory phosphorylation was induced during mitotic exit in CDC20-depleted cells. The expression of an siRNA-resistant CDC20 rescued both the mitotic exit delay and the CDK1-inhibitory phosphorylation. Moreover, the expression of a nonphosphorylatable CDK1 mutant or the downregulation of WEE1 and MYT1 abolished mitotic exit in CDC20-depleted cells. These findings indicate that, in the absence of sufficient APC/C activity, an alternative mechanism that utilized the classic inhibitory phosphorylation of CDK1 could mediate mitotic exit. |
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Authors:
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Jeremy P H Chow; Randy Y C Poon; Hoi Tang Ma |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-01-24 |
Journal Detail:
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Title: Molecular and cellular biology Volume: 31 ISSN: 1098-5549 ISO Abbreviation: Mol. Cell. Biol. Publication Date: 2011 Apr |
Date Detail:
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Created Date: 2011-03-17 Completed Date: 2011-05-16 Revised Date: 2012-04-27 |
Medline Journal Info:
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Nlm Unique ID: 8109087 Medline TA: Mol Cell Biol Country: United States |
Other Details:
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Languages: eng Pagination: 1478-91 Citation Subset: IM |
Affiliation:
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Division of Life Science, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Anaphase CDC2 Protein Kinase / antagonists & inhibitors*, metabolism Cell Cycle Proteins / metabolism Cyclin B1 / metabolism Cytoprotection DNA-Binding Proteins / metabolism Down-Regulation HeLa Cells Humans Microscopy Mitosis* Nuclear Proteins / metabolism Phosphorylation Protein Processing, Post-Translational Protein-Tyrosine Kinases / metabolism Substrate Specificity Time-Lapse Imaging Transcription Factors / metabolism Ubiquitin-Protein Ligase Complexes / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Cell Cycle Proteins; 0/Cyclin B1; 0/DNA-Binding Proteins; 0/MYT1 protein, human; 0/Nuclear Proteins; 0/Transcription Factors; 156288-95-8/CDC20 protein, human; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.10.2/WEE1 protein, human; EC 2.7.11.22/CDC2 Protein Kinase; EC 6.3.2.19/Ubiquitin-Protein Ligase Complexes; EC 6.3.2.19/anaphase-promoting complex |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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