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注意:仅列出部分参考文献,下载原文获取全部文献信息。Telomere dysfunction as a cause of genomic instability in Werner syndrome
Laure Crabbe et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2007)
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Elevated telomere-telomere recombination in WRN-deficient, telomere dystunctional cells promotes escape from senescence and engagement of the ALT pathway
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Mechanisms of common fragile site instability
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Current advances in unraveling the function of the Werner syndrome protein
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Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions
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The Fanconi anemia pathway is required for the DNA replication stress response and for the regulation of common fragile site stability
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Saccharomyces cerevisiae rrm3p DNA helicase promotes genome integrity by preventing replication fork stalling:: Viability of rrm3 cells requires the intra-S-phase checkpoint and fork restart activities
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Local chromatin structure at the ribosomal DNA causes replication fork pausin and genome instability in the absence of the S-cerevisiae DNA helicase Rrm3p
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Werner syndrome protein and the MRE11 complex are involved in a common pathway of replication fork recovery
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BRCA1 is required for common-fragile-site stability via its G2/M checkpoint function
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The Werner syndrome helicase and exonuclease cooperate to resolve telomeric D loops in a manner regulated by TRF1 and TRF2
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Linkage between Werner syndrome protein and the Mre11 complex via Nbs1
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The Werner syndrome protein has separable recombination and survival functions
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The Saccharomyces cerevisiae helicase Rrm3p facilitates replication past nonhistone protein-DNA complexes
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WRN interacts physically and functionally with the recombination mediator protein RAD52
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Werner's syndrome protein is phosphorylated in an ATR/ATM-dependent manner following replication arrest and DNA damage induced during the S phase of the cell cycle
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ATR regulates fragile site stability
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Homologous recombination resolution defect in Werner syndrome
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Biochemical characterization of the DNA substrate specificity of Werner syndrome helicase
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Saccharomyces Rrm3p, a 5′ to 3′ DNA helicase that promotes replication fork progression through telomeric and subtelomeric DNA
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The Mre11 complex is required for repair of hairpin-capped double-strand breaks and prevention of chromosome rearrangements
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RT Abraham
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Werner's syndrome protein is required for correct recovery after replication arrest and DNA damage induced in S-phase of cell cycle
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The Bloom's and Werner's syndrome proteins are DNA structure-specific helicases
P Mohaghegh et al.
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Interactions between the Werner syndrome helicase and DNA polymerase δ specifically facilitate copying of tetraplex and hairpin structures of the d(CGG)n trinucleotide repeat sequence
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Werner helicase relocates into nuclear foci in response to DNA damaging agents and co-localizes with RPA and Rad51
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Werner syndrome cells are sensitive to DNA crosslinking drugs
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DNA damage-dependent nuclear dynamics of the Mre11 complex
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Werner's syndrome cell lines are hypersensitive to camptothecin-induced chromosomal damage
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Lessons from human progeroid syndromes
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Werner's syndrome lymphoblastoid cells are hypersensitive to topoisomerase II inhibitors in the G2 phase of the cell cycle
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The Saccharomyces Pif1p DNA helicase and the highly related Rrm3p have opposite effects on replication fork progression in ribosomal DNA
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Werner syndrome exonuclease catalyzes structure-dependent degradation of DNA
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