Статті в журналах: "A-to-I RNA editing"

1

Wulff, Bjorn‐Erik, and Kazuko Nishikura. "Substitutional A‐to‐I RNA editing." Wiley Interdisciplinary Reviews: RNA 1, no. 1 (May 21, 2010): 90–101. http://dx.doi.org/10.1002/wrna.10.

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2

Schaffer, Amos A., Eli Kopel, Ayal Hendel, Ernesto Picardi, Erez Y. Levanon, and Eli Eisenberg. "The cell line A-to-I RNA editing catalogue." Nucleic Acids Research 48, no. 11 (May 8, 2020): 5849–58. http://dx.doi.org/10.1093/nar/gkaa305.

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Abstract Adenosine-to-inosine (A-to-I) RNA editing is a common post transcriptional modification. It has a critical role in protecting against false activation of innate immunity by endogenous double stranded RNAs and has been associated with various regulatory processes and diseases such as autoimmune and cardiovascular diseases as well as cancer. In addition, the endogenous A-to-I editing machinery has been recently harnessed for RNA engineering. The study of RNA editing in humans relies heavily on the usage of cell lines as an important and commonly-used research tool. In particular, manipulations of the editing enzymes and their targets are often developed using cell line platforms. However, RNA editing in cell lines behaves very differently than in normal and diseased tissues, and most cell lines exhibit low editing levels, requiring over-expression of the enzymes. Here, we explore the A-to-I RNA editing landscape across over 1000 human cell lines types and show that for almost every editing target of interest a suitable cell line that mimics normal tissue condition may be found. We provide CLAIRE, a searchable catalogue of RNA editing levels across cell lines available at http://srv00.recas.ba.infn.it/atlas/claire.html, to facilitate rational choice of appropriate cell lines for future work on A-to-I RNA editing.

3

Sapiro, Anne L., Anat Shmueli, Gilbert Lee Henry, Qin Li, Tali Shalit, Orly Yaron, Yoav Paas, Jin Billy Li, and Galit Shohat-Ophir. "Illuminating spatial A-to-I RNA editing signatures within theDrosophilabrain." Proceedings of the National Academy of Sciences 116, no. 6 (January 18, 2019): 2318–27. http://dx.doi.org/10.1073/pnas.1811768116.

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Adenosine-to-inosine (A-to-I) RNA editing, catalyzed by ADAR enzymes, is a ubiquitous mechanism that generates transcriptomic diversity. This process is particularly important for proper neuronal function; however, little is known about how RNA editing is dynamically regulated between the many functionally distinct neuronal populations of the brain. Here, we present a spatial RNA editing map in theDrosophilabrain and show that different neuronal populations possess distinct RNA editing signatures. After purifying and sequencing RNA from genetically marked groups of neuronal nuclei, we identified a large number of editing sites and compared editing levels in hundreds of transcripts across nine functionally different neuronal populations. We found distinct editing repertoires for each population, including sites in repeat regions of the transcriptome and differential editing in highly conserved and likely functional regions of transcripts that encode essential neuronal genes. These changes are site-specific and not driven by changes inAdarexpression, suggesting a complex, targeted regulation of editing levels in key transcripts. This fine-tuning of the transcriptome between different neurons by RNA editing may account for functional differences between distinct populations in the brain.

4

Maas, Stefan, Yukio Kawahara, Kristen M. Tamburro, and Kazuko Nishikura. "A-to-I RNA Editing and Human Disease." RNA Biology 3, no. 1 (January 2006): 1–9. http://dx.doi.org/10.4161/rna.3.1.2495.

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5

Garrett, Sandra C., and Joshua J. C. Rosenthal. "A Role for A-to-I RNA Editing in Temperature Adaptation." Physiology 27, no. 6 (December 2012): 362–69. http://dx.doi.org/10.1152/physiol.00029.2012.

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A-to-I RNA editing can recode mRNAs, giving organisms the option to express diverse, functionally distinct protein isoforms. Here, we propose that RNA editing is inherently geared for temperature adaptation because it tends to recode to smaller, less stabilizing amino acids. Studies on how editing affects protein function support this idea.

6

Larsen, Knud, and Mads Peter Heide-Jørgensen. "Conservation of A-to-I RNA editing in bowhead whale and pig." PLOS ONE 16, no. 12 (December 9, 2021): e0260081. http://dx.doi.org/10.1371/journal.pone.0260081.

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RNA editing is a post-transcriptional process in which nucleotide changes are introduced into an RNA sequence, many of which can contribute to proteomic sequence variation. The most common type of RNA editing, contributing to nearly 99% of all editing events in RNA, is A-to-I (adenosine-to-inosine) editing mediated by double-stranded RNA-specific adenosine deaminase (ADAR) enzymes. A-to-I editing at ‘recoding’ sites results in non-synonymous substitutions in protein-coding sequences. Here, we present studies of the conservation of A-to-I editing in selected mRNAs between pigs, bowhead whales, humans and two shark species. All examined mRNAs–NEIL1, COG3, GRIA2, FLNA, FLNB, IGFBP7, AZIN1, BLCAP, GLI1, SON, HTR2C and ADAR2 –showed conservation of A-to-I editing of recoding sites. In addition, novel editing sites were identified in NEIL1 and GLI1 in bowhead whales. The A-to-I editing site of human NEIL1 in position 242 was conserved in the bowhead and porcine homologues. A novel editing site was discovered in Tyr244. Differential editing was detected at the two adenosines in the NEIL1 242 codon in both pig and bowhead NEIL1 mRNAs in various tissues and organs. No conservation of editing of KCNB1 and EEF1A mRNAs was seen in bowhead whales. In silico analyses revealed conservation of five adenosines in ADAR2, some of which are subject to A-to-I editing in bowheads and pigs, and conservation of a regulatory sequence in GRIA2 mRNA that is responsible for recognition of the ADAR editing enzyme.

7

Buchumenski, Ilana, Karoline Holler, Lior Appelbaum, Eli Eisenberg, Jan Philipp Junker, and Erez Y. Levanon. "Systematic identification of A-to-I RNA editing in zebrafish development and adult organs." Nucleic Acids Research 49, no. 8 (April 19, 2021): 4325–37. http://dx.doi.org/10.1093/nar/gkab247.

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Abstract A-to-I RNA editing is a common post transcriptional mechanism, mediated by the Adenosine deaminase that acts on RNA (ADAR) enzymes, that increases transcript and protein diversity. The study of RNA editing is limited by the absence of editing maps for most model organisms, hindering the understanding of its impact on various physiological conditions. Here, we mapped the vertebrate developmental landscape of A-to-I RNA editing, and generated the first comprehensive atlas of editing sites in zebrafish. Tens of thousands unique editing events and 149 coding sites were identified with high-accuracy. Some of these edited sites are conserved between zebrafish and humans. Sequence analysis of RNA over seven developmental stages revealed high levels of editing activity in early stages of embryogenesis, when embryos rely on maternal mRNAs and proteins. In contrast to the other organisms studied so far, the highest levels of editing were detected in the zebrafish ovary and testes. This resource can serve as the basis for understanding of the role of editing during zebrafish development and maturity.

8

Washburn, Michael C., and Heather A. Hundley. "Transandcisfactors affecting A-to-I RNA editing efficiency of a noncoding editing target inC. elegans." RNA 22, no. 5 (February 25, 2016): 722–28. http://dx.doi.org/10.1261/rna.055079.115.

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9

Han, Jian, Omer An, HuiQi Hong, Tim Hon Man Chan, Yangyang Song, Haoqing Shen, Sze Jing Tang, et al. "Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression." Science Advances 6, no. 25 (June 2020): eaba5136. http://dx.doi.org/10.1126/sciadv.aba5136.

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RNA editing introduces nucleotide changes in RNA sequences. Recent studies have reported that aberrant A-to-I RNA editing profiles are implicated in cancers. Albeit changes in expression and activity of ADAR genes are thought to have been responsible for the dysregulated RNA editome in diseases, they are not always correlated, indicating the involvement of secondary regulators. Here, we uncover DAP3 as a potent repressor of editing and a strong oncogene in cancer. DAP3 mainly interacts with the deaminase domain of ADAR2 and represses editing via disrupting association of ADAR2 with its target transcripts. PDZD7, an exemplary DAP3-repressed editing target, undergoes a protein recoding editing at stop codon [Stop →Trp (W)]. Because of editing suppression by DAP3, the unedited PDZD7WT, which is more tumorigenic than edited PDZD7Stop518W, is accumulated in tumors. In sum, cancer cells may acquire malignant properties for their survival advantage through suppressing RNA editome by DAP3.

10

Silvestris, Domenico Alessandro, Chiara Scopa, Sara Hanchi, Franco Locatelli, and Angela Gallo. "De Novo A-to-I RNA Editing Discovery in lncRNA." Cancers 12, no. 10 (October 13, 2020): 2959. http://dx.doi.org/10.3390/cancers12102959.

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Background: Adenosine to inosine (A-to-I) RNA editing is the most frequent editing event in humans. It converts adenosine to inosine in double-stranded RNA regions (in coding and non-coding RNAs) through the action of the adenosine deaminase acting on RNA (ADAR) enzymes. Long non-coding RNAs, particularly abundant in the brain, account for a large fraction of the human transcriptome, and their important regulatory role is becoming progressively evident in both normal and transformed cells. Results: Herein, we present a bioinformatic analysis to generate a comprehensive inosinome picture in long non-coding RNAs (lncRNAs), using an ad hoc index and searching for de novo editing events in the normal brain cortex as well as in glioblastoma, a highly aggressive human brain cancer. We discovered >10,000 new sites and 335 novel lncRNAs that undergo editing, never reported before. We found a generalized downregulation of editing at multiple lncRNA sites in glioblastoma samples when compared to the normal brain cortex. Conclusion: Overall, our study discloses a novel layer of complexity that controls lncRNAs in the brain and brain cancer.

11

Marceca, Gioacchino P., Luisa Tomasello, Rosario Distefano, Mario Acunzo, Carlo M. Croce, and Giovanni Nigita. "Detecting and Characterizing A-To-I microRNA Editing in Cancer." Cancers 13, no. 7 (April 3, 2021): 1699. http://dx.doi.org/10.3390/cancers13071699.

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Adenosine to inosine (A-to-I) editing consists of an RNA modification where single adenosines along the RNA sequence are converted into inosines. Such a biochemical transformation is catalyzed by enzymes belonging to the family of adenosine deaminases acting on RNA (ADARs) and occurs either co- or post-transcriptionally. The employment of powerful, high-throughput detection methods has recently revealed that A-to-I editing widely occurs in non-coding RNAs, including microRNAs (miRNAs). MiRNAs are a class of small regulatory non-coding RNAs (ncRNAs) acting as translation inhibitors, known to exert relevant roles in controlling cell cycle, proliferation, and cancer development. Indeed, a growing number of recent researches have evidenced the importance of miRNA editing in cancer biology by exploiting various detection and validation methods. Herein, we briefly overview early and currently available A-to-I miRNA editing detection and validation methods and discuss the significance of A-to-I miRNA editing in human cancer.

12

Franzén, Oscar, Raili Ermel, Katyayani Sukhavasi, Rajeev Jain, Anamika Jain, Christer Betsholtz, Chiara Giannarelli, et al. "Global analysis of A-to-I RNA editing reveals association with common disease variants." PeerJ 6 (March 6, 2018): e4466. http://dx.doi.org/10.7717/peerj.4466.

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RNA editing modifies transcripts and may alter their regulation or function. In humans, the most common modification is adenosine to inosine (A-to-I). We examined the global characteristics of RNA editing in 4,301 human tissue samples. More than 1.6 million A-to-I edits were identified in 62% of all protein-coding transcripts. mRNA recoding was extremely rare; only 11 novel recoding sites were uncovered. Thirty single nucleotide polymorphisms from genome-wide association studies were associated with RNA editing; one that influences type 2 diabetes (rs2028299) was associated with editing in ARPIN. Twenty-five genes, including LRP11 and PLIN5, had editing sites that were associated with plasma lipid levels. Our findings provide new insights into the genetic regulation of RNA editing and establish a rich catalogue for further exploration of this process.

13

Kwak, Shin. "Inefficient A-to-I RNA editing and ALS." Rinsho Shinkeigaku 50, no. 11 (2010): 978. http://dx.doi.org/10.5692/clinicalneurol.50.978.

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14

Xiang, Jian-Feng, Qin Yang, Chu-Xiao Liu, Man Wu, Ling-Ling Chen, and Li Yang. "N6-Methyladenosines Modulate A-to-I RNA Editing." Molecular Cell 69, no. 1 (January 2018): 126–35. http://dx.doi.org/10.1016/j.molcel.2017.12.006.

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15

Mansi, Luigi, Marco Antonio Tangaro, Claudio Lo Giudice, Tiziano Flati, Eli Kopel, Amos Avraham Schaffer, Tiziana Castrignanò, Giovanni Chillemi, Graziano Pesole, and Ernesto Picardi. "REDIportal: millions of novel A-to-I RNA editing events from thousands of RNAseq experiments." Nucleic Acids Research 49, no. D1 (October 26, 2020): D1012—D1019. http://dx.doi.org/10.1093/nar/gkaa916.

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Abstract RNA editing is a relevant epitranscriptome phenomenon able to increase the transcriptome and proteome diversity of eukaryotic organisms. ADAR mediated RNA editing is widespread in humans in which millions of A-to-I changes modify thousands of primary transcripts. RNA editing has pivotal roles in the regulation of gene expression or modulation of the innate immune response or functioning of several neurotransmitter receptors. Massive transcriptome sequencing has fostered the research in this field. Nonetheless, different aspects of the RNA editing biology are still unknown and need to be elucidated. To support the study of A-to-I RNA editing we have updated our REDIportal catalogue raising its content to about 16 millions of events detected in 9642 human RNAseq samples from the GTEx project by using a dedicated pipeline based on the HPC version of the REDItools software. REDIportal now allows searches at sample level, provides overviews of RNA editing profiles per each RNAseq experiment, implements a Gene View module to look at individual events in their genic context and hosts the CLAIRE database. Starting from this novel version, REDIportal will start collecting non-human RNA editing changes for comparative genomics investigations. The database is freely available at http://srv00.recas.ba.infn.it/atlas/index.html.

16

Terajima, Hideki, Mijia Lu, Linda Zhang, Qi Cui, Yanhong Shi, Jianrong Li, and Chuan He. "N6-methyladenosine promotes induction of ADAR1-mediated A-to-I RNA editing to suppress aberrant antiviral innate immune responses." PLOS Biology 19, no. 7 (July 29, 2021): e3001292. http://dx.doi.org/10.1371/journal.pbio.3001292.

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Among over 150 distinct RNA modifications, N6-methyladenosine (m6A) and adenosine-to-inosine (A-to-I) RNA editing represent 2 of the most studied modifications on mammalian mRNAs. Although both modifications occur on adenosine residues, knowledge on potential functional crosstalk between these 2 modifications is still limited. Here, we show that the m6A modification promotes expression levels of the ADAR1, which encodes an A-to-I RNA editing enzyme, in response to interferon (IFN) stimulation. We reveal that YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) mediates up-regulation of ADAR1; YTHDF1 is a reader protein that can preferentially bind m6A-modified transcripts and promote translation. Knockdown of YTHDF1 reduces the overall levels of IFN-induced A-to-I RNA editing, which consequently activates dsRNA-sensing pathway and increases expression of various IFN-stimulated genes. Physiologically, YTHDF1 deficiency inhibits virus replication in cells through regulating IFN responses. The A-to-I RNA editing activity of ADAR1 plays important roles in the YTHDF1-dependent IFN responses. Therefore, we uncover that m6A and YTHDF1 affect innate immune responses through modulating the ADAR1-mediated A-to-I RNA editing.

17

Liddicoat, Brian, Robert Piskol, Alistair Chalk, Miyoko Higuchi, Peter Seeburg, Jin Billy Li, Jochen Hartner, and Carl R. Walkley. "A-To-I RNA Editing By ADAR1 Is Essential For Hematopoiesis." Blood 122, no. 21 (November 15, 2013): 1199. http://dx.doi.org/10.1182/blood.v122.21.1199.1199.

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Abstract The role of RNA and its regulation is becoming increasingly appreciated as a vital component of hematopoietic development. RNA editing by members of the Adenosine Deaminase Acting on RNA (ADAR) gene family is a form of post-transcriptional modification which converts genomically encoded adenosine to inosine (A-to-I) in double-stranded RNA. A-to-I editing by ADAR directly converts the sequence of the RNA substrate and can alter the structure, function, processing, and localization of the targeted RNA. ADAR1 is ubiquitously expressed and we have previously described essential roles in the development of hematopoietic and hepatic organs. Germline ablation of murine ADAR1 results in a significant upregulation of interferon (IFN) stimulated genes and embryonic death between E11.5 and E12.5 associated with fetal liver disintegration and failed hemopoiesis. To determine the biological importance of A-to-I editing by ADAR1, we generated an editing dead knock-in allele of ADAR1 (ADAR1E861A). Mice homozygous for the ADAR1E861A allele died in utero at ∼E13.5. The fetal liver (FL) was small and had significantly lower cellularity than in controls. Analysis of hemopoiesis demonstrated increased apoptosis and a loss of hematopoietic stem cells (HSC) and all mature lineages. Most notably erythropoiesis was severely impaired with ∼7-fold reduction across all erythrocyte progenitor populations compared to controls. These data are consistent with our previous findings that ADAR1 is essential for erythropoiesis (unpublished data) and suggest that the ADAR1E861A allele phenocopies the null allele in utero. To assess the requirement of A-to-I editing in adult hematopoiesis, we generated mice where we could somatically delete the wild-type ADAR1 allele and leave only ADAR1E861A expressed in HSCs (hScl-CreERAdar1fl/E861A). In comparison to hScl-CreERAdar1fl/+ controls, hScl-CreERAdar1fl/E861A mice were anemic and had severe leukopenia 20 days post tamoxifen treatment. Investigation of marrow hemopoiesis revealed a significant loss of all cells committed to the erythroid lineage in hScl-CreERAdar1fl/E861A mice, despite having elevated phenotypic HSCs. Upon withdrawal of tamoxifen diet, all blood parameters were restored to control levels within 12 weeks owing to strong selection against cells expressing only the ADAR1E861A allele. To understand the mechanism through which ADAR1 mediated A-to-I editing regulates hematopoiesis, RNA-seq was performed. Gene expression profiles showed that a loss of ADAR1 mediated A-to-I editing resulted in a significant upregulation of IFN signatures, consistent with the gene expression changes in ADAR1 null mice. To define substrates of ADAR1 we assessed A-to-I mismatches in the RNA-seq data sets. 3,560 previously known and 353 novel A-to-I editing sites were identified in our data set. However, no single editing substrate discovered could account for the IFN signature observed or the lethality of ADAR1E861A/E861A mice. These results demonstrate that ADAR1 mediated A-to-I editing is essential for the maintenance of both fetal and adult hemopoiesis in a cell-autonomous manner and a key suppressor of the IFN response in hematopoiesis. Furthermore the ADAR1E861A allele demonstrates the essential role of ADAR1 in vivo is A-to-I editing. Disclosures: Hartner: TaconicArtemis: Employment.

18

Haas, Roni, Nabeel Ganem, Ayya Keshet, Angela Orlov, Alla Fishman, and Ayelet Lamm. "A-to-I RNA Editing Affects lncRNAs Expression after Heat Shock." Genes 9, no. 12 (December 13, 2018): 627. http://dx.doi.org/10.3390/genes9120627.

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Adenosine to inosine (A-to-I) RNA editing is a highly conserved regulatory process carried out by adenosine-deaminases (ADARs) on double-stranded RNA (dsRNAs). Although a considerable fraction of the transcriptome is edited, the function of most editing sites is unknown. Previous studies indicate changes in A-to-I RNA editing frequencies following exposure to several stress types. However, the overall effect of stress on the expression of ADAR targets is not fully understood. Here, we performed high-throughput RNA sequencing of wild-type and ADAR mutant Caenorhabditis elegans worms after heat-shock to analyze the effect of heat-shock stress on the expression pattern of genes. We found that ADAR regulation following heat-shock does not directly involve heat-shock related genes. Our analysis also revealed that long non-coding RNAs (lncRNAs) and pseudogenes, which have a tendency for secondary RNA structures, are enriched among upregulated genes following heat-shock in ADAR mutant worms. The same group of genes is downregulated in ADAR mutant worms under permissive conditions, which is likely, considering that A-to-I editing protects endogenous dsRNA from RNA-interference (RNAi). Therefore, temperature increases may destabilize dsRNA structures and protect them from RNAi degradation, despite the lack of ADAR function. These findings shed new light on the dynamics of gene expression under heat-shock in relation to ADAR function.

19

Liu, Huiquan, Yang Li, Daipeng Chen, Zhaomei Qi, Qinhu Wang, Jianhua Wang, Cong Jiang, and Jin-Rong Xu. "A-to-I RNA editing is developmentally regulated and generally adaptive for sexual reproduction in Neurospora crassa." Proceedings of the National Academy of Sciences 114, no. 37 (August 28, 2017): E7756—E7765. http://dx.doi.org/10.1073/pnas.1702591114.

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Although fungi lack adenosine deaminase acting on RNA (ADAR) enzymes, adenosine to inosine (A-to-I) RNA editing was reported recently in Fusarium graminearum during sexual reproduction. In this study, we profiled the A-to-I editing landscape and characterized its functional and adaptive properties in the model filamentous fungus Neurospora crassa. A total of 40,677 A-to-I editing sites were identified, and approximately half of them displayed stage-specific editing or editing levels at different sexual stages. RNA-sequencing analysis with the Δstc-1 and Δsad-1 mutants confirmed A-to-I editing occurred before ascus development but became more prevalent during ascosporogenesis. Besides fungal-specific sequence and secondary structure preference, 63.5% of A-to-I editing sites were in the coding regions and 81.3% of them resulted in nonsynonymous recoding, resulting in a significant increase in the proteome complexity. Many genes involved in RNA silencing, DNA methylation, and histone modifications had extensive recoding, including sad-1, sms-3, qde-1, and dim-2. Fifty pseudogenes harbor premature stop codons that require A-to-I editing to encode full-length proteins. Unlike in humans, nonsynonymous editing events in N. crassa are generally beneficial and favored by positive selection. Almost half of the nonsynonymous editing sites in N. crassa are conserved and edited in Neurospora tetrasperma. Furthermore, hundreds of them are conserved in F. graminearum and had higher editing levels. Two unknown genes with editing sites conserved between Neurospora and Fusarium were experimentally shown to be important for ascosporogenesis. This study comprehensively analyzed A-to-I editing in N. crassa and showed that RNA editing is stage-specific and generally adaptive, and may be functionally related to repeat induced point mutation and meiotic silencing by unpaired DNA.

20

Gallo, Angela, and Silvia Galardi. "A-to-I RNA editing and cancer: From pathology to basic science." RNA Biology 5, no. 3 (July 2008): 135–39. http://dx.doi.org/10.4161/rna.5.3.6739.

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21

Pozdyshev, Denis V., Anastasia A. Zharikova, Maria V. Medvedeva, and Vladimir I. Muronetz. "Differential Analysis of A-to-I mRNA Edited Sites in Parkinson’s Disease." Genes 13, no. 1 (December 22, 2021): 14. http://dx.doi.org/10.3390/genes13010014.

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Parkinson’s disease (PD) is a widespread neuronal degenerative disorder with unexplored etiology. It is associated with various pathological events. In particular, the prefrontal cortex Brodmann area 9 (BA9) region is affected in PD. This frontal lobe brain region plays an important role in cognitive, motor, and memory-related functions. BA9 develops Lewy bodies in PD patients and shows essential changes in transcriptome and proteome, connected with mitochondria related pathways, protein folding pathways, and metallothioneins. Recently, altered adenosine to inosine mRNA editing patterns have been detected in various neurological pathologies. In this article, we present an investigation of differences in A-to-I RNA editing levels and specificity of mRNA editing sites in brain tissues of healthy and PD patients based on RNA sequencing data. Overall, decreased editing levels in the brains of PD patients were observed, potential editing sites with altered editing during PD were identified, and the role of different adenosine deaminases in this process was analyzed.

22

Nevo-Caspi, Yael, Ninette Amariglio, Gideon Rechavi, and Gideon Paret. "A-to-I RNA Editing is Induced Upon Hypoxia." Shock 35, no. 6 (June 2011): 585–89. http://dx.doi.org/10.1097/shk.0b013e31820fe4b7.

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23

Duan, Yuange, Shengqian Dou, Shiqi Luo, Hong Zhang, and Jian Lu. "Adaptation of A-to-I RNA editing in Drosophila." PLOS Genetics 13, no. 3 (March 10, 2017): e1006648. http://dx.doi.org/10.1371/journal.pgen.1006648.

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24

Shtrichman, Ronit, Igal Germanguz, Rachel Mandel, Anna Ziskind, Irit Nahor, Michal Safran, Sivan Osenberg, Ofra Sherf, Gideon Rechavi, and Joseph Itskovitz-Eldor. "Altered A-to-I RNA Editing in Human Embryogenesis." PLoS ONE 7, no. 7 (July 31, 2012): e41576. http://dx.doi.org/10.1371/journal.pone.0041576.

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25

Eisenberg, Eli, Sergey Nemzer, Yaron Kinar, Rotem Sorek, Gideon Rechavi, and Erez Y. Levanon. "Is abundant A-to-I RNA editing primate-specific?" Trends in Genetics 21, no. 2 (February 2005): 77–81. http://dx.doi.org/10.1016/j.tig.2004.12.005.

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26

Picardi, Ernesto, Luigi Mansi, and Graziano Pesole. "Detection of A-to-I RNA Editing in SARS-COV-2." Genes 13, no. 1 (December 23, 2021): 41. http://dx.doi.org/10.3390/genes13010041.

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ADAR1-mediated deamination of adenosines in long double-stranded RNAs plays an important role in modulating the innate immune response. However, recent investigations based on metatranscriptomic samples of COVID-19 patients and SARS-COV-2-infected Vero cells have recovered contrasting findings. Using RNAseq data from time course experiments of infected human cell lines and transcriptome data from Vero cells and clinical samples, we prove that A-to-G changes observed in SARS-COV-2 genomes represent genuine RNA editing events, likely mediated by ADAR1. While the A-to-I editing rate is generally low, changes are distributed along the entire viral genome, are overrepresented in exonic regions, and are (in the majority of cases) nonsynonymous. The impact of RNA editing on virus–host interactions could be relevant to identify potential targets for therapeutic interventions.

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Bhakta, Sonali, and Toshifumi Tsukahara. "C-to-U RNA Editing: A Site Directed RNA Editing Tool for Restoration of Genetic Code." Genes 13, no. 9 (September 12, 2022): 1636. http://dx.doi.org/10.3390/genes13091636.

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The restoration of genetic code by editing mutated genes is a potential method for the treatment of genetic diseases/disorders. Genetic disorders are caused by the point mutations of thymine (T) to cytidine (C) or guanosine (G) to adenine (A), for which gene editing (editing of mutated genes) is a promising therapeutic technique. In C-to-Uridine (U) RNA editing, it converts the base C-to-U in RNA molecules and leads to nonsynonymous changes when occurring in coding regions; however, for G-to-A mutations, A-to-I editing occurs. Editing of C-to-U is not as physiologically common as that of A-to-I editing. Although hundreds to thousands of coding sites have been found to be C-to-U edited or editable in humans, the biological significance of this phenomenon remains elusive. In this review, we have tried to provide detailed information on physiological and artificial approaches for C-to-U RNA editing.

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Goncharov, Anton O., Victoria O. Shender, Ksenia G. Kuznetsova, Anna A. Kliuchnikova, and Sergei A. Moshkovskii. "Interplay between A-to-I Editing and Splicing of RNA: A Potential Point of Application for Cancer Therapy." International Journal of Molecular Sciences 23, no. 9 (May 8, 2022): 5240. http://dx.doi.org/10.3390/ijms23095240.

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Adenosine-to-inosine RNA editing is a system of post-transcriptional modification widely distributed in metazoans which is catalyzed by ADAR enzymes and occurs mostly in double-stranded RNA (dsRNA) before splicing. This type of RNA editing changes the genetic code, as inosine generally pairs with cytosine in contrast to adenosine, and this expectably modulates RNA splicing. We review the interconnections between RNA editing and splicing in the context of human cancer. The editing of transcripts may have various effects on splicing, and resultant alternatively spliced isoforms may be either tumor-suppressive or oncogenic. Dysregulated RNA splicing in cancer often causes the release of excess amounts of dsRNA into cytosol, where specific dsRNA sensors provoke antiviral-like responses, including type I interferon signaling. These responses may arrest cell division, causing apoptosis and, externally, stimulate antitumor immunity. Thus, small-molecule spliceosome inhibitors have been shown to facilitate the antiviral-like signaling and are considered to be potential cancer therapies. In turn, a cytoplasmic isoform of ADAR can deaminate dsRNA in cytosol, thereby decreasing its levels and diminishing antitumor innate immunity. We propose that complete or partial inhibition of ADAR may enhance the proapoptotic and cytotoxic effects of splicing inhibitors and that it may be considered a promising addition to cancer therapies targeting RNA splicing.

29

Song, Yulong, Xiuju He, Wenbing Yang, Yaoxing Wu, Jun Cui, Tian Tang, and Rui Zhang. "Virus-specific editing identification approach reveals the landscape of A-to-I editing and its impacts on SARS-CoV-2 characteristics and evolution." Nucleic Acids Research 50, no. 5 (March 2, 2022): 2509–21. http://dx.doi.org/10.1093/nar/gkac120.

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Abstract Upon SARS-CoV-2 infection, viral intermediates specifically activate the IFN response through MDA5-mediated sensing and accordingly induce ADAR1 p150 expression, which might lead to viral A-to-I RNA editing. Here, we developed an RNA virus-specific editing identification pipeline, surveyed 7622 RNA-seq data from diverse types of samples infected with SARS-CoV-2, and constructed an atlas of A-to-I RNA editing sites in SARS-CoV-2. We found that A-to-I editing was dynamically regulated, varied between tissue and cell types, and was correlated with the intensity of innate immune response. On average, 91 editing events were deposited at viral dsRNA intermediates per sample. Moreover, editing hotspots were observed, including recoding sites in the spike gene that affect viral infectivity and antigenicity. Finally, we provided evidence that RNA editing accelerated SARS-CoV-2 evolution in humans during the epidemic. Our study highlights the ability of SARS-CoV-2 to hijack components of the host antiviral machinery to edit its genome and fuel its evolution, and also provides a framework and resource for studying viral RNA editing.

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Heale, Bret S. E., Ana Eulalio, Leon Schulte, Jörg Vogel, and Mary A. O’Connell. "Analysis of A to I editing of miRNA in macrophages exposed to Salmonella." RNA Biology 7, no. 5 (September 2010): 621–27. http://dx.doi.org/10.4161/rna.7.5.13269.

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31

Heraud-Farlow, Jacki E., and Carl R. Walkley. "What do editors do? Understanding the physiological functions of A-to-I RNA editing by adenosine deaminase acting on RNAs." Open Biology 10, no. 7 (July 2020): 200085. http://dx.doi.org/10.1098/rsob.200085.

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Adenosine-to-inosine (A-to-I) editing is a post-transcriptional modification of RNA which changes its sequence, coding potential and secondary structure. Catalysed by the adenosine deaminase acting on RNA (ADAR) proteins, ADAR1 and ADAR2, A-to-I editing occurs at approximately 50 000–150 000 sites in mice and into the millions of sites in humans. The vast majority of A-to-I editing occurs in repetitive elements, accounting for the discrepancy in total numbers of sites between species. The species-conserved primary role of editing by ADAR1 in mammals is to suppress innate immune activation by unedited cell-derived endogenous RNA. In the absence of editing, inverted paired sequences, such as Alu elements, are thought to form stable double-stranded RNA (dsRNA) structures which trigger activation of dsRNA sensors, such as MDA5. A small subset of editing sites are within coding sequences and are evolutionarily conserved across metazoans. Editing by ADAR2 has been demonstrated to be physiologically important for recoding of neurotransmitter receptors in the brain. Furthermore, changes in RNA editing are associated with various pathological states, from the severe autoimmune disease Aicardi-Goutières syndrome, to various neurodevelopmental and psychiatric conditions and cancer. However, does detection of an editing site imply functional importance? Genetic studies in humans and genetically modified mouse models together with evolutionary genomics have begun to clarify the roles of A-to-I editing in vivo . Furthermore, recent developments suggest there may be the potential for distinct functions of editing during pathological conditions such as cancer.

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Abudayyeh, Omar O., Jonathan S. Gootenberg, Brian Franklin, Jeremy Koob, Max J. Kellner, Alim Ladha, Julia Joung, Paul Kirchgatterer, David B. T. Cox, and Feng Zhang. "A cytosine deaminase for programmable single-base RNA editing." Science 365, no. 6451 (July 11, 2019): 382–86. http://dx.doi.org/10.1126/science.aax7063.

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Programmable RNA editing enables reversible recoding of RNA information for research and disease treatment. Previously, we developed a programmable adenosine-to-inosine (A-to-I) RNA editing approach by fusing catalytically inactivate RNA-targeting CRISPR-Cas13 (dCas13) with the adenine deaminase domain of ADAR2. Here, we report a cytidine-to-uridine (C-to-U) RNA editor, referred to as RNA Editing for Specific C-to-U Exchange (RESCUE), by directly evolving ADAR2 into a cytidine deaminase. RESCUE doubles the number of mutations targetable by RNA editing and enables modulation of phosphosignaling-relevant residues. We apply RESCUE to drive β-catenin activation and cellular growth. Furthermore, RESCUE retains A-to-I editing activity, enabling multiplexed C-to-U and A-to-I editing through the use of tailored guide RNAs.

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RING, HENRIK, HENRIK BOIJE, CHAMMIRAN DANIEL, JOHAN OHLSON, MARIE ÖHMAN та FINN HALLBÖÖK. "Increased A-to-I RNA editing of the transcript for GABAA receptor subunit α3 during chick retinal development". Visual Neuroscience 27, № 5-6 (16 вересня 2010): 149–57. http://dx.doi.org/10.1017/s0952523810000180.

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AbstractAdenosine-to-inosine (A-to-I) RNA editing is a cotranscriptional or posttranscriptional gene regulatory mechanism that increases the diversity of the proteome in the nervous system. Recently, the transcript for GABA type A receptor subunit α3 was found to be subjected to RNA editing. The aim of this study was to determine if editing of the chicken α3 subunit transcript occurs in the retina and if the editing is temporally regulated during development. We also raised the question if editing of the α3 transcript was temporally associated with the suggested developmental shift from excitation to inhibition in the GABA system. The editing frequency was studied by using Sanger and Pyrosequencing, and to monitor the temporal aspects, we studied the messenger RNA expression of the GABAA receptor subunits and chloride pumps, known to be involved in the switch. The results showed that the chick α3 subunit was subjected to RNA editing, and its expression was restricted to cells in the inner nuclear and ganglion cell layer in the retina. The extent of editing increased during development (after embryonic days 8–9) concomitantly with an increase of expression of the chloride pump KCC2. Expression of several GABAA receptor subunits known to mediate synaptic GABA actions was upregulated at this time. We conclude that editing of the chick GABAA subunit α3 transcript in chick retina gives rise to an amino acid change that may be of importance in the switch from excitatory to inhibitory receptors.

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Wang, Zishuai, Xikang Feng, Zhonglin Tang, and Shuai Cheng Li. "Genome-Wide Investigation and Functional Analysis of Sus scrofa RNA Editing Sites across Eleven Tissues." Genes 10, no. 5 (April 30, 2019): 327. http://dx.doi.org/10.3390/genes10050327.

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Recently, the prevalence and importance of RNA editing have been illuminated in mammals. However, studies on RNA editing of pigs, a widely used biomedical model animal, are rare. Here we collected RNA sequencing data across 11 tissues and identified more than 490,000 RNA editing sites. We annotated their biological features, detected flank sequence characteristics of A-to-I editing sites and the impact of A-to-I editing on miRNA–mRNA interactions, and identified RNA editing quantitative trait loci (edQTL). Sus scrofa RNA editing sites showed high enrichment in repetitive regions with a median editing level as 15.38%. Expectedly, 96.3% of the editing sites located in non-coding regions including intron, 3′ UTRs, intergenic, and gene proximal regions. There were 2233 editing sites located in the coding regions and 980 of them caused missense mutation. Our results indicated that to an A-to-I editing site, the adjacent four nucleotides, two before it and two after it, have a high impact on the editing occurrences. A commonly observed editing motif is CCAGG. We found that 4552 A-to-I RNA editing sites could disturb the original binding efficiencies of miRNAs and 4176 A-to-I RNA editing sites created new potential miRNA target sites. In addition, we performed edQTL analysis and found that 1134 edQTLs that significantly affected the editing levels of 137 RNA editing sites. Finally, we constructed PRESDB, the first pig RNA editing sites database. The site provides necessary functions associated with Sus scrofa RNA editing study.

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Hosaka, Takashi, Hiroshi Tsuji, and Shin Kwak. "RNA Editing: A New Therapeutic Target in Amyotrophic Lateral Sclerosis and Other Neurological Diseases." International Journal of Molecular Sciences 22, no. 20 (October 11, 2021): 10958. http://dx.doi.org/10.3390/ijms222010958.

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The conversion of adenosine to inosine in RNA editing (A-to-I RNA editing) is recognized as a critical post-transcriptional modification of RNA by adenosine deaminases acting on RNAs (ADARs). A-to-I RNA editing occurs predominantly in mammalian and human central nervous systems and can alter the function of translated proteins, including neurotransmitter receptors and ion channels; therefore, the role of dysregulated RNA editing in the pathogenesis of neurological diseases has been speculated. Specifically, the failure of A-to-I RNA editing at the glutamine/arginine (Q/R) site of the GluA2 subunit causes excessive permeability of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors to Ca2+, inducing fatal status epilepticus and the neurodegeneration of motor neurons in mice. Therefore, an RNA editing deficiency at the Q/R site in GluA2 due to the downregulation of ADAR2 in the motor neurons of sporadic amyotrophic lateral sclerosis (ALS) patients suggests that Ca2+-permeable AMPA receptors and the dysregulation of RNA editing are suitable therapeutic targets for ALS. Gene therapy has recently emerged as a new therapeutic opportunity for many heretofore incurable diseases, and RNA editing dysregulation can be a target for gene therapy; therefore, we reviewed neurological diseases associated with dysregulated RNA editing and a new therapeutic approach targeting dysregulated RNA editing, especially one that is effective in ALS.

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Tian, N., X. Wu, Y. Zhang, and Y. Jin. "A-to-I editing sites are a genomically encoded G: Implications for the evolutionary significance and identification of novel editing sites." RNA 14, no. 2 (December 14, 2007): 211–16. http://dx.doi.org/10.1261/rna.797108.

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37

Peng, Xinxin, Xiaoyan Xu, Yumeng Wang, David H. Hawke, Shuangxing Yu, Leng Han, Zhicheng Zhou, et al. "A-to-I RNA Editing Contributes to Proteomic Diversity in Cancer." Cancer Cell 33, no. 5 (May 2018): 817–28. http://dx.doi.org/10.1016/j.ccell.2018.03.026.

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Cayir, Akin. "RNA A-to-I editing, environmental exposure, and human diseases." Critical Reviews in Toxicology 51, no. 5 (May 28, 2021): 456–66. http://dx.doi.org/10.1080/10408444.2021.1953438.

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39

Ganem, Nabeel S., and Ayelet T. Lamm. "A-to-I RNA editing – thinking beyond the single nucleotide." RNA Biology 14, no. 12 (October 11, 2017): 1690–94. http://dx.doi.org/10.1080/15476286.2017.1364830.

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40

Eisenberg, Eli, and Erez Y. Levanon. "A-to-I RNA editing — immune protector and transcriptome diversifier." Nature Reviews Genetics 19, no. 8 (April 24, 2018): 473–90. http://dx.doi.org/10.1038/s41576-018-0006-1.

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41

Yablonovitch, Arielle L., Patricia Deng, Dionna Jacobson, and Jin Billy Li. "The evolution and adaptation of A-to-I RNA editing." PLOS Genetics 13, no. 11 (November 28, 2017): e1007064. http://dx.doi.org/10.1371/journal.pgen.1007064.

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42

Maas, Stefan, Alexander Rich, and Kazuko Nishikura. "A-to-I RNA Editing: Recent News and Residual Mysteries." Journal of Biological Chemistry 278, no. 3 (November 20, 2002): 1391–94. http://dx.doi.org/10.1074/jbc.r200025200.

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43

Shallev, Lea, Eli Kopel, Ariel Feiglin, Gil S. Leichner, Dror Avni, Yechezkel Sidi, Eli Eisenberg, Aviv Barzilai, Erez Y. Levanon, and Shoshana Greenberger. "Decreased A-to-I RNA editing as a source of keratinocytes' dsRNA in psoriasis." RNA 24, no. 6 (March 28, 2018): 828–40. http://dx.doi.org/10.1261/rna.064659.117.

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44

Samuel, Charles E. "Adenosine deaminase acting on RNA (ADAR1), a suppressor of double-stranded RNA–triggered innate immune responses." Journal of Biological Chemistry 294, no. 5 (February 1, 2019): 1710–20. http://dx.doi.org/10.1074/jbc.tm118.004166.

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Herbert “Herb” Tabor, who celebrated his 100th birthday this past year, served the Journal of Biological Chemistry as a member of the Editorial Board beginning in 1961, as an Associate Editor, and as Editor-in-Chief for 40 years, from 1971 until 2010. Among the many discoveries in biological chemistry during this period was the identification of RNA modification by C6 deamination of adenosine (A) to produce inosine (I) in double-stranded (ds) RNA. This posttranscriptional RNA modification by adenosine deamination, known as A-to-I RNA editing, diversifies the transcriptome and modulates the innate immune interferon response. A-to-I editing is catalyzed by a family of enzymes, adenosine deaminases acting on dsRNA (ADARs). The roles of A-to-I editing are varied and include effects on mRNA translation, pre-mRNA splicing, and micro-RNA silencing. Suppression of dsRNA-triggered induction and action of interferon, the cornerstone of innate immunity, has emerged as a key function of ADAR1 editing of self (cellular) and nonself (viral) dsRNAs. A-to-I modification of RNA is essential for the normal regulation of cellular processes. Dysregulation of A-to-I editing by ADAR1 can have profound consequences, ranging from effects on cell growth and development to autoimmune disorders.

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Ramaswami, Gokul, and Jin Billy Li. "RADAR: a rigorously annotated database of A-to-I RNA editing." Nucleic Acids Research 42, no. D1 (October 25, 2013): D109—D113. http://dx.doi.org/10.1093/nar/gkt996.

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46

Weirick, Tyler, Giuseppe Militello, Mohammed Rabiul Hosen, David John, Joseph B. Moore, and Shizuka Uchida. "Investigation of RNA Editing Sites within Bound Regions of RNA-Binding Proteins." High-Throughput 8, no. 4 (November 29, 2019): 19. http://dx.doi.org/10.3390/ht8040019.

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Studies in epitranscriptomics indicate that RNA is modified by a variety of enzymes. Among these RNA modifications, adenosine to inosine (A-to-I) RNA editing occurs frequently in the mammalian transcriptome. These RNA editing sites can be detected directly from RNA sequencing (RNA-seq) data by examining nucleotide changes from adenosine (A) to guanine (G), which substitutes for inosine (I). However, a careful investigation of such nucleotide changes must be conducted to distinguish sequencing errors and genomic mutations from the genuine editing sites. Building upon our recent introduction of an easy-to-use bioinformatics tool, RNA Editor, to detect RNA editing events from RNA-seq data, we examined the extent by which RNA editing events affect the binding of RNA-binding proteins (RBP). Through employing bioinformatic techniques, we uncovered that RNA editing sites occur frequently in RBP-bound regions. Moreover, the presence of RNA editing sites are more frequent when RNA editing islands were examined, which are regions in which RNA editing sites are present in clusters. When the binding of one RBP, human antigen R [HuR; encoded by ELAV-like protein 1 (ELAV1)], was quantified experimentally, its binding was reduced upon silencing of the RNA editing enzyme adenosine deaminases acting on RNA (ADAR) compared to the control—suggesting that the presence of RNA editing islands influence HuR binding to its target regions. These data indicate RNA editing as an important mediator of RBP–RNA interactions—a mechanism which likely constitutes an additional mode of post-transcription gene regulation in biological systems.

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Duan, Yuange, Wanzhi Cai, and Hu Li. "Chloroplast C-to-U RNA editing in vascular plants is adaptive due to its restorative effect: testing the restorative hypothesis." RNA 29, no. 2 (January 17, 2023): 141–52. http://dx.doi.org/10.1261/rna.079450.122.

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The adaptiveness of nonsynonymous RNA editing (recoding) could be conferred by the flexibility of the temporal-spatially controllable proteomic diversity, or by its restorative effect which fixes unfavorable genomic mutations at the RNA level. These two complementary hypotheses, namely, the diversifying hypothesis and the restorative hypothesis, have distinct predictions on the landscape of RNA editing sites. We collected the chloroplast C-to-U RNA editomes of 21 vascular plants (11 angiosperms, four gymnosperms, and six ferns) from a previous study, aiming to testify whether the plant editomes typically conform to the restorative hypothesis. All predictions made by the restorative hypothesis are verified: (i) nonsynonymous editing sites are more frequent and have higher editing levels than synonymous sites; (ii) nonsynonymous editing levels are extremely high and show weak tissue-specificity in plants; (iii) on the inferred genomic sites with recent T-to-C mutations, nonsynonymous sites but not synonymous sites are compensated by C-to-U RNA editing. In conclusion, nonsynonymous C-to-U RNA editing in plants is adaptive due to its restorative effects. The recoding levels are high and are constantly required across the whole plant so that the recoding events could perfectly mimic DNA mutations. The evolutionary significance of plant RNA editing is systematically demonstrated at the genome-wide level.

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Kwak, Shin, Yoshinori Nishimoto, and Takenari Yamashita. "Newly identified ADAR-mediated A-to-I editing positions as a tool for ALS research." RNA Biology 5, no. 4 (October 2008): 193–97. http://dx.doi.org/10.4161/rna.6925.

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Choyon, Alif, Ashiqur Rahman, Md Hasanuzzaman, Dewan Md Farid, and Swakkhar Shatabda. "PRESa2i: incremental decision trees for prediction of Adenosine to Inosine RNA editing sites." F1000Research 9 (April 16, 2020): 262. http://dx.doi.org/10.12688/f1000research.22823.1.

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RNA editing is a very crucial cellular process affecting protein encoding and is sometimes correlated with the cause of fatal diseases, such as cancer. Thus knowledge about RNA editing sites in a RNA sequence is very important. Adenosine to Inosine (A-to-I) is the most common of the RNA editing events. In this paper,we present PRESa2i, a computation prediction tool for identification of A-to-I RNA editing sites in given RNA sequences. PRESa2i uses a simple, yet effective set of sequence based features generated from RNA sequences and a novel feature selection technique. It uses an incremental decision tree algorithm as the classification algorithm. On a standard benchmark dataset and independent set, it achieves 86.48% accuracy and 90.67% sensitivity and significantly outperforms state-of-the-art methods. We have also implemented a web application based on PRESa2i and made it available freely at: http://brl.uiu.ac.bd/presa2i/index.php. The materials for this paper are also available to use from: https://github.com/swakkhar/RNA-Editing/.

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Irimia, Manuel, Amanda Denuc, Jose L. Ferran, Barbara Pernaute, Luis Puelles, Scott W. Roy, Jordi Garcia-Fernàndez, and Gemma Marfany. "Evolutionarily conserved A-to-I editing increases protein stability of the alternative splicing factorNova1." RNA Biology 9, no. 1 (January 2012): 12–21. http://dx.doi.org/10.4161/rna.9.1.18387.

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