Current Strategies for Site-Directed RNA editing using ADARs
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TLDR
Though the precise and efficient re-direction of ADAR activity still remains a challenge, the systems that are being developed lay the foundation for SDRE as a powerful tool for transient genome editing.About:
This article is published in Methods.The article was published on 2019-03-01 and is currently open access. It has received 44 citations till now. The article focuses on the topics: RNA editing & ADAR.read more
Citations
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Journal ArticleDOI
Genome-wide quantification of ADAR adenosine-to-inosine RNA editing activity.
TL;DR: The Alu editing index (AEI) quantifies genome-wide editing in Alu repeats and allows comparison across samples, and is used to map global editing across a large dataset of healthy human samples and identify putative regulators of ADAR.
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CRISPR-Cas13 Inhibitors Block RNA Editing in Bacteria and Mammalian Cells
Ping Lin,Ping Lin,Shugang Qin,Shugang Qin,Qinqin Pu,Qinqin Pu,Zhihan Wang,Zhihan Wang,Qun Wu,Qun Wu,Pan Gao,Pan Gao,Jacob Schettler,Kai Guo,Rongpeng Li,Guoping Li,Canhua Huang,Yuquan Wei,George F. Gao,Jianxin Jiang,Min Wu +20 more
TL;DR: Using integrated approaches to screen acrVI candidates and evaluate their effects on Cas13 function, a series of acrVIA1-7 genes that block the activities of Cas13a are discovered and may enable precise RNA editing in Cas13-based application and study of phage-bacterium interaction.
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Functions and consequences of AID/APOBEC-mediated DNA and RNA deamination
TL;DR: Pecori et al. as discussed by the authors provide an overview of the AID/APOBEC cytidine deaminase family, discussing key structural features, how they contribute to viral and tumour evolution and how they can be harnessed for (potentially therapeutic) base-editing purposes.
Journal ArticleDOI
In vivo repair of a protein underlying a neurological disorder by programmable RNA editing
John R. Sinnamon,Susan Y. Kim,Jenna R. Fisk,Zhen Song,Hiroyuki Nakai,Sophia Jeng,Shannon K. McWeeney,Gail Mandel +7 more
TL;DR: It is demonstrated that programmable RNA editing can be utilized to repair mutations in mouse models of neurological disease and a guanosine-to-adenosine mutation in methyl CpG binding protein 2 RNA that causes Rett syndrome is successfully repaired.
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Adenosine-to-inosine RNA editing in neurological development and disease
TL;DR: Adenosine-to-inosine (A-toI) editing is one of the most prevalent post-transcriptional RNA modifications in metazoan as mentioned in this paper, which is catalysed by enzymes called adenosine deaminases acting on RNs.
References
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The DNA Damage Response: Making It Safe to Play with Knives
TL;DR: This review will focus on how the DDR controls DNA repair and the phenotypic consequences of defects in these critical regulatory functions in mammals.
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High-frequency off-target mutagenesis induced by CRISPR-Cas nucleases in human cells.
Yanfang Fu,Jennifer A Foden,Cyd Khayter,Morgan L. Maeder,Deepak Reyon,J. Keith Joung,Jeffry D. Sander +6 more
TL;DR: It is found that single and double mismatches are tolerated to varying degrees depending on their position along the guide RNA (gRNA)-DNA interface, and off-target cleavage of CRISPR-associated (Cas)9-based RGNs is characterized.
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CRISPR-Cas systems for editing, regulating and targeting genomes
Jeffry D. Sander,J. Keith Joung +1 more
TL;DR: A modified version of the CRISPR-Cas9 system has been developed to recruit heterologous domains that can regulate endogenous gene expression or label specific genomic loci in living cells, which will undoubtedly transform biological research and spur the development of novel molecular therapeutics for human disease.
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A general method for the covalent labeling of fusion proteins with small molecules in vivo
TL;DR: A general method for the covalent labeling of fusion proteins in vivo that complements existing methods for noncovalentlabeling of proteins and that may open up new ways of studying proteins in living cells is described.
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Playing the End Game: DNA Double-Strand Break Repair Pathway Choice
TL;DR: Recent insights are reviewed into the mechanisms that influence the choice between competing DSB repair pathways, how this is regulated during the cell cycle, and how imbalances in this equilibrium result in genome instability.