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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

ATR Regulates Fragile Site Stability

TL;DR: It is proposed that fragile sites are unreplicated chromosomal regions resulting from stalled forks that escape the ATR replication checkpoint, and have important implications for understanding both the mechanism of fragile site instability and the consequences of stalled replication in mammalian cells.
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Multiple mechanisms control chromosome integrity after replication fork uncoupling and restart at irreparable UV lesions.

TL;DR: It is proposed that the coordinated action of checkpoint, recombination, and translesion synthesis-mediated processes at the fork and behind the fork preserves the integrity of replicating chromosomes by allowing efficient replication restart and filling the resulting ssDNA gaps.
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Mrc1 transduces signals of DNA replication stress to activate Rad53.

TL;DR: Mrc1 mutants are sensitive to hydroxyurea and have a checkpoint defect similar to rad53 and cds1 mutants, which may be the replicative counterpart of Rad9 and Crb2, which are required for activating ScRad53 and Chk1 in response to DNA damage.
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Crosstalk between SUMO and ubiquitin on PCNA is mediated by recruitment of the helicase Srs2p.

TL;DR: It is shown that Srs2p physically interacts with sumoylated PCNA, which contributes to the recruitment of the helicase to replication forks, suggesting a mechanism by which SUMO and ubiquitin cooperatively control the choice of pathway for the processing of DNA lesions during replication.
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ATR Homolog Mec1 Promotes Fork Progression, Thus Averting Breaks in Replication Slow Zones

TL;DR: Yeast Mec1 has important functions in normal S phase and the genome instability of mec1(and, analogously, ATR −/−) mutants stems from defects in these basic roles.
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