| Dissecting the role of ubiquitylation in the DNA damage response checkpoint in G2. | |
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MedLine Citation:
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PMID: 19680264 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Maintenance of genomic integrity is one of the fundamental biological properties shared by all living organisms. To counterbalance deleterious and potentially mutagenic effects of omnipresent DNA damaging assaults, organisms have developed a network of genome surveillance and maintenance pathways known as the DNA damage response. In eukaryotes, the orchestration of cell-cycle checkpoints, DNA damage repair, and apoptosis in response to DNA damage relies on posttranslational modifications of key regulatory proteins. Although the role of phosphorylation in these pathways is relatively well established, the significance of ubiquitylation has only recently emerged. In this review, we survey current research on the ubiquitin-proteasome system, focusing on the DNA damage response in the G2 phase of the cell cycle and two prominent classes of ubiquitin ligases, the SCF- and APC/C complexes. These ubiquitin ligases are reviewed with regard to their function in activating, maintaining, and terminating the checkpoint and in light of increasing evidence that suggests a dynamic balance of substrate ubiquitylation and deubiquitylation. We further discuss the impact of defective G2 checkpoint signaling on genomic stability and cancer risk, highlighting strategies for targeted antitumor drug discovery. |
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Authors:
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F Bassermann; M Pagano |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Cell death and differentiation Volume: 17 ISSN: 1476-5403 ISO Abbreviation: Cell Death Differ. Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2009-12-16 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9437445 Medline TA: Cell Death Differ Country: England |
Other Details:
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Languages: eng Pagination: 78-85 Citation Subset: IM |
Affiliation:
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Department of Medicine III, Technical University of Munich, Munich, Germany. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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