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Journal ArticleDOI

RADX controls RAD51 filament dynamics to regulate replication fork stability.

TLDR
In this paper, a single-strand DNA (ssDNA) binding protein that regulates DNA replication, called RADX, is defined and its mechanism of action, and it is shown that RADX directly and selectively interacts with ATP-bound RAD51, stimulates ATP hydrolysis and destabilizes RAD51 nucleofilaments.
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This article is published in Molecular Cell.The article was published on 2021-03-04. It has received 15 citations till now. The article focuses on the topics: Replication fork reversal & DNA replication.

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Citations
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Journal ArticleDOI

RAD52: Paradigm of Synthetic Lethality and New Developments

TL;DR: In this article, the authors have shown that mammalian RAD52 is critical for backup DNA repair pathways in HR-deficient cancer cells, which makes RAD52 an attractive target for the development of anti-cancer therapies against BRCAdeficient cancers.
Journal ArticleDOI

Replication Fork Reversal and Protection

TL;DR: A review on the key factors and mechanisms required for the remodeling and protection of stalled replication forks in mammalian cells can be found in this paper, where the authors also discuss the role of DNA damage repair proteins.
Journal ArticleDOI

RADX prevents genome instability by confining replication fork reversal to stalled forks.

TL;DR: 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.
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The Emerging Roles of Rad51 in Cancer and Its Potential as a Therapeutic Target

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

RAD51 paralogs: Expanding roles in replication stress responses and repair.

TL;DR: In this article , the authors highlight the recent findings that uncovered the novel functions of RAD51 paralogs in replication fork progression, its stability, and restart and discuss RAD51-paralogs as a potential therapeutic target for cancer treatment.
References
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Journal ArticleDOI

Comparative Protein Structure Modeling Using MODELLER

TL;DR: This unit describes how to calculate comparative models using the program MODELLER and discusses all four steps of comparative modeling, frequently observed errors, and some applications.
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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.
Journal ArticleDOI

Insights into DNA recombination from the structure of a RAD51-BRCA2 complex

TL;DR: The BRC repeat mimics a motif in RAD51 that serves as an interface for oligomerization between individual RAD51 monomers, thus enabling BRCA2 to control the assembly of the RAD51 nucleoprotein filament, which is essential for strand-pairing reactions during DNA recombination.
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Purified human BRCA2 stimulates RAD51-mediated recombination

TL;DR: The purification of full-length BRCA2 is reported and it is shown that it both binds RAD51 and potentiates recombinational DNA repair by promoting assembly of RAD51 onto single-stranded DNA (ssDNA).
Journal ArticleDOI

Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells

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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