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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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Genome editing with CRISPR–Cas nucleases, base editors, transposases and prime editors

TL;DR: This work analyzes key considerations when choosing genome editing agents and identifies opportunities for future improvements and applications in basic research and therapeutics.
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Gene therapy returns to centre stage

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CRISPR-Cas guides the future of genetic engineering.

TL;DR: The basic mechanisms that set the CRISPR-Cas toolkit apart from other programmable gene-editing technologies are described, highlighting the diverse and naturally evolved systems now functionalized as biotechnologies.
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Homologous Recombination and Human Health: The Roles of BRCA1, BRCA2, and Associated Proteins

TL;DR: This review summarizes recent findings on BRCA1, BRCa2, and associated proteins involved in human disease with an emphasis on their molecular roles and interactions.
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Recombination, Pairing, and Synapsis of Homologs during Meiosis

TL;DR: This review provides an overview of recombination-mediated processes in physical and functional linkage with meiotic axial chromosome structure, with interplay in both directions, before, during, and after formation and dissolution of the synaptonemal complex.
References
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Journal ArticleDOI

Ubc13/Rnf8 ubiquitin ligases control foci formation of the Rap80/Abraxas/Brca1/Brcc36 complex in response to DNA damage

TL;DR: An FHA domain RING finger E3 ubiquitin ligase, RNF8, and an E2-conjugating enzyme known to form K63–polyubiquitin chains, Ubc13, each of which is required to recruit the Brca1 A complex to sites of DNA damage are identified.
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Model for homologous recombination during transfer of DNA into mouse L cells: role for DNA ends in the recombination process.

TL;DR: A model to explain how recombination might occur in mammalian cells is proposed and it is shown that both intramolecular and intermolecular homologous recombination can be detected after gene transfer and the degree of recombination decreases with decreasing tk gene homology.
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Group I introns as mobile genetic elements: facts and mechanistic speculations--a review.

TL;DR: Mechanisms of intron acquisition and intron loss must create an equilibrium, which explains the irregular distribution of group I introns in various genetic systems and predicts that horizontal transfer ofintron sequences must occur between unrelated species, using vectors yet to be discovered.
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The SUMO modification pathway is involved in the BRCA1 response to genotoxic stress

TL;DR: It is reported that BRCA1 is modified by small ubiquitin-like modifier (SUMO) in response to genotoxic stress, and co-localizes at sites of DNA damage with SUMO1, SUMO2/3 and the SUMO-conjugating enzyme Ubc9.
Journal ArticleDOI

Colocalization of multiple DNA double-strand breaks at a single Rad52 repair centre.

TL;DR: Analysis of DNA damage checkpoint-deficient cells provides direct evidence for coordination between DNA repair and subsequent release from checkpoint arrest and analyses of cells experiencing multiple DSBs demonstrate that Rad52 foci are centres of DNA repair capable of simultaneously recruiting more than one DSB.
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