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Journal ArticleDOI

Interplay of replication checkpoints and repair proteins at stalled replication forks.

Dana Branzei, +1 more
- 01 Jul 2007 - 
- Vol. 6, Iss: 7, pp 994-1003
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TLDR
This review focuses mainly on the results obtained in budding yeast on the multiple roles of checkpoints in maintaining fork integrity and on the enzymatic activities that cooperate with the checkpoint pathway to promote fork resumption and repair of DNA lesions thereby contributing to genome integrity.
About
This article is published in DNA Repair.The article was published on 2007-07-01. It has received 144 citations till now. The article focuses on the topics: Control of chromosome duplication & DNA re-replication.

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Citations
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An oncogene-induced DNA damage model for cancer development.

TL;DR: Oncogene-induced DNA damage may explain two key features of cancer: genomic instability and the high frequency of p53 mutations.
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The DNA Damage Response: Ten Years After

TL;DR: This work has witnessed an explosion in understanding of DNA damage sensing, signaling, and the complex interplay between protein phosphorylation and the ubiquitin pathway employed by the DDR network to execute the response to DNA damage.
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Mechanism of eukaryotic homologous recombination.

TL;DR: HR accessory factors that facilitate other stages of the Rad51- and Dmc1-catalyzed homologous DNA pairing and strand exchange reaction have also been identified.
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Regulation of DNA repair throughout the cell cycle

TL;DR: The repair of DNA lesions that occur endogenously or in response to diverse genotoxic stresses is indispensable for genome integrity and has provided insights into the mechanisms that contribute to DNA repair in specific cell-cycle phases.
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Hydroxyurea-Stalled Replication Forks Become Progressively Inactivated and Require Two Different RAD51-Mediated Pathways for Restart and Repair

TL;DR: The XRCC3 protein, which is required for RAD51 foci formation, is also required for replication restart of HU-stalled forks, suggesting that RAD51-mediated strand invasion supports fork restart.
References
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Journal ArticleDOI

Rad51-dependent DNA structures accumulate at damaged replication forks in sgs1 mutants defective in the yeast ortholog of BLM RecQ helicase.

TL;DR: It is suggested that, in sgs1 cells, the unscheduled accumulation of Rad51-dependent cruciform structures at damaged forks result from defective maturation of recombination-dependent intermediates that originate from the replication-related sister chromatid junctions.
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Human DNA Polymerase η Promotes DNA Synthesis from Strand Invasion Intermediates of Homologous Recombination

TL;DR: The results indicate a dual function for poleta at stalled replication forks: the promotion of translesion synthesis and the reinitiation of DNA synthesis by homologous recombination repair.
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A Rad53 Kinase-Dependent Surveillance Mechanism that Regulates Histone Protein Levels in S. cerevisiae

TL;DR: This work shows that rad53, but not mec1 mutants, are extremely sensitive to histone overexpression, as Rad53 is required for degradation of excess histones, resulting in slow growth, DNA damage sensitivity, and chromosome loss phenotypes that are significantly suppressed by a reduction in histone gene dosage.
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Suppression of Spontaneous Chromosomal Rearrangements by S Phase Checkpoint Functions in Saccharomyces cerevisiae

TL;DR: Data suggest that one role of S phase checkpoint functions in normal cells is to suppress spontaneous genome rearrangements resulting from DNA replication errors.
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Specific complex formation between yeast RAD6 and RAD18 proteins: A potential mechanism for targeting RAD6 ubiquitin-conjugating activity to DNA damage sites

TL;DR: Whereas RAD6 has no affinity for DNA, RAD18 binds single-stranded DNA, and association of RAD6 with RAD18 could provide a means for targeting RAD6 to damage-containing DNA regions, where the RAD6 ubiquitin-conjugating function could modulate the activity of a stalled DNA replication machinery.
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