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dc.contributor.authorGrudic, Amraen_US
dc.contributor.authorJul-Larsen, Åsneen_US
dc.contributor.authorHaring, SJen_US
dc.contributor.authorWold, MSen_US
dc.contributor.authorLønning, Per Eysteinen_US
dc.contributor.authorBjerkvig, Rolfen_US
dc.contributor.authorBøe, Stig Oveen_US
dc.PublishedNucleic Acids Research 2007, 35(21):7267-7278eng
dc.description.abstractThe activation of a telomere maintenance mechanism is required for cancer development in humans. While most tumors achieve this by expressing the enzyme telomerase, a fraction (5–15%) employs a recombination-based mechanism termed alternative lengthening of telomeres (ALT). Here we show that loss of the single-stranded DNA-binding protein replication protein A (RPA) in human ALT cells, but not in telomerase-positive cells, causes increased exposure of single-stranded G-rich telomeric DNA, cell cycle arrest in G2/M phase, accumulation of single-stranded telomeric DNA within ALT-associated PML bodies (APBs), and formation of telomeric aggregates at the ends of metaphase chromosomes. This study demonstrates differences between ALT cells and telomerase-positive cells in the requirement for RPA in telomere processing and implicates the ALT mechanism in tumor cells as a possible therapeutic target.en_US
dc.publisherOxford University Press (OUP)eng
dc.rightsAttribution CC BY-NC 2.0 UKeng
dc.titleReplication protein A prevents accumulation of single-stranded telomeric DNA in cells that use alternative lengthening of telomeresen_US
dc.typePeer reviewed
dc.typeJournal article
dc.rights.holderCopyright 2007 The Author(s)
dc.subject.nsiVDP::Medisinske Fag: 700en_US

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Attribution CC BY-NC 2.0 UK
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