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pubmed-article:20950945pubmed:abstractTextThe backup pathway of nonhomologous end joining (B-NHEJ) enables cells to process DNA double-strand breaks (DSBs) when the DNA-PK-dependent pathway of NHEJ (D-NHEJ) is compromised. Our previous results show marked reduction in the activity of B-NHEJ when LIG4(-/-) mouse embryo fibroblasts (MEFs) cease to grow and enter a plateau phase. The dependence of B-NHEJ on growth state is substantially stronger than that of D-NHEJ and points to regulatory mechanisms or processing determinants that require elucidation. Because the different D-NHEJ mutants show phenotypes distinct in their details, it is necessary to characterize the dependence of their DSB repair capacity on growth state and to explore species-specific responses.lld:pubmed
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pubmed-article:20950945pubmed:authorpubmed-author:ZhangLihuaLlld:pubmed
pubmed-article:20950945pubmed:authorpubmed-author:WangMinliMlld:pubmed
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pubmed-article:20950945pubmed:authorpubmed-author:WuWenqiWlld:pubmed
pubmed-article:20950945pubmed:copyrightInfoCopyright © 2011 Elsevier Inc. All rights reserved.lld:pubmed
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pubmed-article:20950945pubmed:articleTitleWidespread dependence of backup NHEJ on growth state: ramifications for the use of DNA-PK inhibitors.lld:pubmed
pubmed-article:20950945pubmed:affiliationInstitute of Medical Radiation Biology, University Duisburg-Essen Medical School, Essen, Germany.lld:pubmed
pubmed-article:20950945pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20950945pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed