Journal ArticleDOI
RADX prevents genome instability by confining replication fork reversal to stalled forks.
Archana Krishnamoorthy,Jessica Jackson,Taha M. Mohamed,Madison B. Adolph,Alessandro Vindigni,David Cortez +5 more
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TLDR
In this article, a single-strand DNA binding protein that binds to and destabilizes RAD51 nucleofilaments, can either inhibit or promote fork reversal depending on replication stress levels.About:
This article is published in Molecular Cell.The article was published on 2021-07-15. It has received 9 citations till now. The article focuses on the topics: Replication fork reversal & DNA replication.read more
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Journal ArticleDOI
Replication stress: from chromatin to immunity and beyond.
Yea-Lih Lin,Philippe Pasero +1 more
TL;DR: A review of the causes and consequences of replication stress in cancer cells can be found in this article, with a focus on endogenous replication impediments and their impact on fork velocity and the interplay between stalled forks and innate immunity.
Journal ArticleDOI
The Emerging Roles of Rad51 in Cancer and Its Potential as a Therapeutic Target
Ziyi Wang,Renxiang Jia,Linlin Wang,Qiwei Yang,Xiao-Di Hu,Qiang Fu,Xinyu Zhang,Wenya Li,Yi Ren +8 more
TL;DR: The structure, expression pattern of Rad 51 and key Rad51 mediators involved in homologous recombination are introduced and the role of Rad51 in tumor metabolism, metastasis, resistance to chemotherapeutic agents and poly-ADP ribose polymerase inhibitors is discussed.
Journal ArticleDOI
Oligomerization of DNA replication regulatory protein RADX is essential to maintain replication fork stability
TL;DR: Cortez et al. as discussed by the authors found that RADX acts as a homo-oligomer to control replication fork stability and that mutations in this region prevent oligomerization and prevent RADX function in cells, and that addition of a heterologous dimerization domain to the oligomerisation mutants restored their ability to regulate replication.
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Non-Recombinogenic Functions of Rad51, BRCA2, and Rad52 in DNA Damage Tolerance.
TL;DR: In this paper, the authors review recent advances showing that Rad51, BRCA2, and Rad52 perform some of these functions through mechanisms that do not require the strand exchange activity of Rad51: the formation and protection of reversed fork structures aimed to bypass blocking lesions, and the promotion of TLS.
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RAD51 bypasses the CMG helicase to promote replication fork reversal
Wenpeng Liu,Yuichiro Saito,Jessica Jackson,Rahul Bhowmick,Masato T. Kanemaki,Alessandro Vindigni,David Cortez +6 more
TL;DR: Jiang et al. as discussed by the authors showed that fork reversal happens while maintaining the helicase in a position poised to restart DNA synthesis and complete genome duplication, which can explain how reversal helps cells tolerate replication stress and rapidly resume DNA synthesis.
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Journal ArticleDOI
Double-strand break repair-independent role for BRCA2 in blocking stalled replication fork degradation by MRE11
TL;DR: Using single-molecule DNA fiber analysis, it is shown that nascent replication tracts created before fork stalling with hydroxyurea are degraded in the absence of BRCA2 but are stable in wild-type cells.
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DNA processing is not required for ATM-mediated telomere damage response after TRF2 deletion.
Giulia B. Celli,Titia de Lange +1 more
TL;DR: Activation of the ATM kinase pathway at chromosome ends does not require overhang degradation or other overt DNA processing, and telomere structure after conditional deletion of mouse TRF2, the protective factor at telomeres is studied.
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Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells
Ralph Zellweger,Damian Dalcher,Karun Mutreja,Matteo Berti,Jonas A. Schmid,Raquel Herrador,Alessandro Vindigni,Massimo Lopes +7 more
TL;DR: Genotoxic treatments in human cells consistently induce uncoupling of replication forks and their remodeling into four-way junctions by the RAD51 recombinase.
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Rad51 protects nascent DNA from Mre11-dependent degradation and promotes continuous DNA synthesis
TL;DR: Direct roles for Rad51 at replication forks are revealed, demonstrating that Rad51 protects newly synthesized DNA from Mre11-dependent degradation and promotes continuous DNA synthesis.
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A forward chemical genetic screen reveals an inhibitor of the Mre11-Rad50-Nbs1 complex
Aude Dupré,Louise Boyer-Chatenet,Louise Boyer-Chatenet,Rose M Sattler,Ami P. Modi,Ji-Hoon Lee,Matthew L. Nicolette,Levy Kopelovich,Maria Jasin,Richard Baer,Tanya T. Paull,Jean Gautier +11 more
TL;DR: It is shown that mirin abolishes the G2/M checkpoint and homology-dependent repair in mammalian cells, and it inhibits Mre11-associated exonuclease activity, consistent with its ability to target the MRN complex.