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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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Journal ArticleDOI

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

DNA end resection, homologous recombination and DNA damage checkpoint activation require CDK1

TL;DR: It is reported that DNA damage checkpoint activation by a DSB requires the cyclin-dependent kinase CDK1 (Cdc28) in budding yeast, andCDK1 is also required for DSB-induced homologous recombination at any cell cycle stage.
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The yeast type I topoisomerase Top3 interacts with Sgs1, a DNA helicase homolog: a potential eukaryotic reverse gyrase.

TL;DR: In this paper, the SGS1 protein was identified as a slow growth suppressor that suppresses both the growth defect and the increased genomic instability of top-3 mutants in Saccharomyces cerevisiae, and it was shown that Sgs1 creates a deleterious topological substrate that Top3 preferentially resolves.
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A Mec1- and Rad53-dependent checkpoint controls late-firing origins of DNA replication

TL;DR: It is shown that, in budding yeast, hydroxyurea, which blocks the progression of replication forks from early-firing origins, also inhibits the firing of late origins, indicating that regulation of late origin firing may also be an important component of the ‘intra-S-phase’ checkpoint and may aid cell survival under adverse conditions.
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Regulation of DNA replication fork progression through damaged DNA by the Mec1/Rad53 checkpoint

TL;DR: It is shown that the DNA-alkylating agent methyl methanesulphonate profoundly reduces the rate of DNA replication fork progression; however, this moderation does not require Rad53 or Mec1 and the accelerated S phase in checkpoint mutants, therefore, is primarily a consequence of inappropriate initiation events.
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S-phase checkpoint proteins Tof1 and Mrc1 form a stable replication-pausing complex

TL;DR: It is demonstrated that the checkpoint regulatory proteins Tof1 and Mrc1 interact directly with the DNA replication machinery in Saccharomyces cerevisiae, which forms a stable pausing structure that serves to anchor subsequent DNA repair events.
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