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Repair of strand breaks by homologous recombination.

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TLDR
The enzymology of the process is discussed, followed by studies on DSB repair in living cells, and a historical context for the current view of HR is provided and how DSBs are processed during HR as well as interactions with other D SB repair pathways are described.
Abstract
In this review, we discuss the repair of DNA double-strand breaks (DSBs) using a homologous DNA sequence (i.e., homologous recombination [HR]), focusing mainly on yeast and mammals. We provide a historical context for the current view of HR and describe how DSBs are processed during HR as well as interactions with other DSB repair pathways. We discuss the enzymology of the process, followed by studies on DSB repair in living cells. Whenever possible, we cite both original articles and reviews to aid the reader for further studies.

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Journal ArticleDOI

Impaired DNA double-strand break repair contributes to the age-associated rise of genomic instability in humans

TL;DR: Rescue experiments indicate that restoration of XRCC4 and Lig4 may suppress the onset of stress-induced premature cellular senescence, suggesting that improving NHEJ efficiency and fidelity by targeting the N HEJ pathway holds great potential to delay aging and mitigate aging-related pathologies.
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When Genome Maintenance Goes Badly Awry

TL;DR: Recent advances in understanding of genetic changes occurring in cancers and the roles of genome maintenance pathways are reviewed.
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DNA polymerase θ (POLQ) is important for repair of DNA double-strand breaks caused by fork collapse.

TL;DR: Evidence is provided to support a novel cancer treatment strategy that combines POLQ inhibition with administration of topoisomerase or ATR inhibitors, which induces replication stress and fork collapse, which may have a significant impact on developing targeted cancer treatment.
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Small-molecule inhibitors identify the RAD52-ssDNA interaction as critical for recovery from replication stress and for survival of BRCA2 deficient cells

TL;DR: Cellular studies with inhibitors showed that the RAD52-ssDNA interaction enables its function at stalled replication forks, and that the inhibition of RAD52 -ssDNA binding acts additively with BRCA2 or MUS81 depletion in cell killing.
References
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Journal ArticleDOI

A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity.

TL;DR: This study reveals a family of endonucleases that use dual-RNAs for site-specific DNA cleavage and highlights the potential to exploit the system for RNA-programmable genome editing.
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Multiplex Genome Engineering Using CRISPR/Cas Systems

TL;DR: The type II prokaryotic CRISPR (clustered regularly interspaced short palindromic repeats)/Cas adaptive immune system has been shown to facilitate RNA-guided site-specific DNA cleavage as discussed by the authors.

Multiplex Genome Engineering Using CRISPR/Cas Systems

TL;DR: Two different type II CRISPR/Cas systems are engineered and it is demonstrated that Cas9 nucleases can be directed by short RNAs to induce precise cleavage at endogenous genomic loci in human and mouse cells, demonstrating easy programmability and wide applicability of the RNA-guided nuclease technology.
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RNA-Guided Human Genome Engineering via Cas9

TL;DR: The type II bacterial CRISPR system is engineer to function with custom guide RNA (gRNA) in human cells to establish an RNA-guided editing tool for facile, robust, and multiplexable human genome engineering.
Journal ArticleDOI

Efficient genome editing in zebrafish using a CRISPR-Cas system

TL;DR: It is shown that the CRISPR-Cas system functions in vivo to induce targeted genetic modifications in zebrafish embryos with efficiencies similar to those obtained using zinc finger nucleases and transcription activator-like effector nucleases.
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