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Search results for: Adars

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#33082451   2020/10/20 To Up

Point mutation bias in SARS-CoV-2 variants results in increased ability to stimulate inflammatory responses.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces severe pneumonia and is the cause of a worldwide pandemic. Coronaviruses, including SARS-CoV-2, have RNA proofreading enzymes in their genomes, resulting in fewer gene mutations than other RNA viruses. Nevertheless, variants of SARS-CoV-2 exist and may induce different symptoms; however, the factors and the impacts of these mutations are not well understood. We found that there is a bias to the mutations occurring in SARS-CoV-2 variants, with disproportionate mutation to uracil (U). These point mutations to U are mainly derived from cytosine (C), which is consistent with the substrate specificity of host RNA editing enzymes, APOBECs. We also found the point mutations which are consistent with other RNA editing enzymes, ADARs. For the C-to-U mutations, the context of the upstream uracil and downstream guanine from mutated position was found to be most prevalent. Further, the degree of increase of U in SARS-CoV-2 variants correlates with enhanced production of cytokines, such as TNF-α and IL-6, in cell lines when compared with stimulation by the ssRNA sequence of the isolated virus in Wuhan. Therefore, RNA editing is a factor for mutation bias in SARS-CoV-2 variants, which affects host inflammatory cytokines production.
Masato Kosuge, Emi Furusawa-Nishii, Koyu Ito, Yoshiro Saito, Kouetsu Ogasawara

1285 related Products with: Point mutation bias in SARS-CoV-2 variants results in increased ability to stimulate inflammatory responses.

1010 mg2ug5ug12ug20ug25ml250ul2000 Units200ul

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#33046702   2020/10/12 To Up

High-throughput mutagenesis reveals unique structural features of human ADAR1.

Adenosine Deaminases that act on RNA (ADARs) are enzymes that catalyze adenosine to inosine conversion in dsRNA, a common form of RNA editing. Mutations in the human ADAR1 gene are known to cause disease and recent studies have identified ADAR1 as a potential therapeutic target for a subset of cancers. However, efforts to define the mechanistic effects for disease associated ADAR1 mutations and the rational design of ADAR1 inhibitors are limited by a lack of structural information. Here, we describe the combination of high throughput mutagenesis screening studies, biochemical characterization and Rosetta-based structure modeling to identify unique features of ADAR1. Importantly, these studies reveal a previously unknown zinc-binding site on the surface of the ADAR1 deaminase domain which is important for ADAR1 editing activity. Furthermore, we present structural models that explain known properties of this enzyme and make predictions about the role of specific residues in a surface loop unique to ADAR1.
SeHee Park, Erin E Doherty, Yixuan Xie, Anil K Padyana, Fang Fang, Yue Zhang, Agya Karki, Carlito B Lebrilla, Justin B Siegel, Peter A Beal

2399 related Products with: High-throughput mutagenesis reveals unique structural features of human ADAR1.

10x96, 2.0ml cultures1 mg96 wells (1 kit)10, 10ml whole blood 96 wells (1 kit)96 Tests/kit96 wells (1 kit)96 wells (1 kit)0.1mg96 tests1ml

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#32962255   2020/09/20 To Up

Altered Regulation of adipomiR Editing with Aging.

Adipose dysfunction with aging increases risk to insulin resistance and other chronic metabolic diseases. We previously showed functional changes in microRNAs involved in pre-adipocyte differentiation with aging resulting in adipose dysfunction. However, the mechanisms leading to this dysfunction in microRNAs in adipose tissue (adipomiRs) during aging are not well understood. We determined the longitudinal changes in expression of adipomiRs and studied their regulatory mechanisms, such as miRNA biogenesis and editing, in an aging rodent model, with Fischer344 × Brown-Norway hybrid rats at ages ranging from 3 to 30 months (male/females, n > 8). Expression of adipomiRs and their edited forms were determined by small-RNA sequencing. RT-qPCR was used to measure the mRNA expression of biogenesis and editing enzymes. Sanger sequencing was used to validate editing with aging. Differential expression of adipomiRs involved in adipocyte differentiation and insulin signaling was altered with aging. Sex- and age-specific changes in edited adipomiRs were observed. An increase in miRNA biogenesis and editing enzymes (ADARs and their splice variants) were observed with increasing age, more so in female than male rats. The adipose dysfunction observed with age is attributed to differences in editing of adipomiRs, suggesting a novel regulatory pathway in aging.
Sabel Meadows, Abbagael Seidler, Madison Wall, Jamika Page, Cara Taylor, Brendin Flinn, Robin Turner, Nalini Santanam

2507 related Products with: Altered Regulation of adipomiR Editing with Aging.

50 ug2 Pieces/Box 50 UG96 wells300 units5 x 50 ug 5 G

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#32729088   // To Up

RNA Editing in Neurological and Neurodegenerative Disorders.

The brain is one of the organs that are preferentially targeted by adenosine-to-inosine (A-to-I) RNA editing, a posttranscriptional modification. This chemical modification affects neuronal development and functions at multiple levels, leading to normal brain homeostasis by increasing the complexity of the transcriptome. This includes modulation of the properties of ion channel and neurotransmitter receptors by recoding, redirection of miRNA targets by changing sequence complementarity, and suppression of immune response by altering RNA structure. Therefore, from another perspective, it appears that the brain is highly vulnerable to dysregulation of A-to-I RNA editing. Here, we focus on how aberrant A-to-I RNA editing is involved in neurological and neurodegenerative diseases of humans including epilepsy, amyotrophic lateral sclerosis, psychiatric disorders, developmental disorders, brain tumors, and encephalopathy caused by autoimmunity. In addition, we provide information regarding animal models to better understand the mechanisms behind disease phenotype.
Pedro Henrique Costa Cruz, Yukio Kawahara

1576 related Products with: RNA Editing in Neurological and Neurodegenerative Disorders.

200ul200ul100 μg100 μg50mg100 ul1 g1 g100ug Lyophilized96 wells

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#32729079   // To Up

ALU A-to-I RNA Editing: Millions of Sites and Many Open Questions.

Alu elements are repetitive short interspersed elements prevalent in the primate genome. These repeats account for over 10% of the genome with more than a million highly similar copies. A direct outcome of this is an enrichment in long structures of stable dsRNA, which are the target of adenosine deaminases acting on RNAs (ADARs), the enzymes catalyzing A-to-I RNA editing. Indeed, A-to-I editing by ADARs is extremely abundant in primates: over a hundred million editing sites exist in their genomes. However, despite the radical increase in ADAR targets brought on by the introduction of Alu elements, the few evolutionary conserved editing sites manage to retain their editing levels. Here, we review and discuss the cost of having an unusual amount of dsRNA and editing in the transcriptome, as well as the opportunities it presents, which possibly contributed to accelerating primate evolution.
Amos A Schaffer, Erez Y Levanon

1842 related Products with: ALU A-to-I RNA Editing: Millions of Sites and Many Open Questions.

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#32729073   // To Up

Discovering RNA Editing Events in Fungi.

RNA editing is an important posttranscriptional process that alters the genetic information of RNA encoded by genomic DNA. Adenosine-to-inosine (A-to-I) editing is the most prevalent type of RNA editing in animal kingdom, catalyzed by adenosine deaminases acting on RNA (ADARs). Recently, genome-wide A-to-I RNA editing is discovered in fungi, involving adenosine deamination mechanisms distinct from animals. Aiming to draw more attention to RNA editing in fungi, here we discuss the considerations for deep sequencing data preparation and the available various methods for detecting RNA editing, with a special emphasis on their usability for fungal RNA editing detection. We describe computational protocols for the identification of candidate RNA editing sites in fungi by using two software packages REDItools and RES-Scanner with RNA sequencing (RNA-Seq) and genomic DNA sequencing (DNA-Seq) data.
Huiquan Liu, Jin-Rong Xu

1896 related Products with: Discovering RNA Editing Events in Fungi.

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#32693003   2020/07/18 To Up

RNA editing mediates the functional switch of COPA in a novel mechanism of hepatocarcinogenesis.

RNA editing introduces nucleotide changes in RNA sequences. Recent studies have reported aberrant adenosine-to-inosine RNA editing is implicated in cancers. Until now, very few functionally important protein-recoding editing targets have been discovered. Here, we investigated the role of a recently discovered protein-recoding editing target COPA (coatomer subunit α) in hepatocellular carcinoma (HCC).
Yangyang Song, Omer An, Xi Ren, Tim Hon Man Chan, Daryl Jin Tai Tay, Sze Jing Tang, Jian Han, HuiQi Hong, Vanessa Hui En Ng, Xinyu Ke, Haoqing Shen, Priyankaa Pitcheshwar, Jaymie Siqi Lin, Ka Wai Leong, Fernando Bellido Molias, Henry Yang, Dennis Kappei, Leilei Chen

2528 related Products with: RNA editing mediates the functional switch of COPA in a novel mechanism of hepatocarcinogenesis.

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#32668759   2020/07/13 To Up

Development of a Single Construct System for Site-Directed RNA Editing Using MS2-ADAR.

Site-directed RNA editing (SDRE) technologies have great potential for treating genetic diseases caused by point mutations. Our group and other researchers have developed SDRE methods utilizing adenosine deaminases acting on RNA (ADARs) and guide RNAs recruiting ADARs to target RNAs bearing point mutations. In general, efficient SDRE relies on introducing numerous guide RNAs relative to target genes. However, achieving a large ratio is not possible for gene therapy applications. In order to achieve a realistic ratio, we herein developed a system that can introduce an equal number of genes and guide RNAs into cultured cells using a fusion protein comprising an ADAR fragment and a plasmid vector containing one copy of each gene on a single construct. We transfected the single construct into HEK293T cells and achieved relatively high efficiency (up to 42%). The results demonstrate that efficient SDRE is possible when the copy number is similar for all three factors (target gene, guide RNA, and ADAR enzyme). This method is expected to be capable of highly efficient gene repair , making it applicable for gene therapy.
Tetsuto Tohama, Matomo Sakari, Toshifumi Tsukahara

1761 related Products with: Development of a Single Construct System for Site-Directed RNA Editing Using MS2-ADAR.

1 G10 ml10 mg100 mg50ml 70 Slides 50 ml100μg0.1 mg1l

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