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Non-VLPs
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
Recently, a first example was presented of engineering the MS2 tethering system to design an RNA editing enzyme complex capable of targeting specific point mutations and restoring the genetic code (Azad et al. 2017, 2019; Bhakta et al. 2018). The authors engineered the deaminase domain of adenosine deaminase acting on RNA (ADAR1) and the MS2 system to target specific adenosines, with the goal of correcting G-to-A mutations at the RNA level. The ADAR1 deaminase domain was fused downstream of the MS2 coat, and the guide RNAs complementary to target RNAs were designed. The guide RNAs directed the ADAR1 deaminase to the desired editing site, where it converted adenosine to inosine. This approach could facilitate the rational use of the ADAR variants for genetic restoration and treatment of genetic diseases. The ADAR recruitment by the MS2 tagging system was reviewed recently by Chen G et al. (2019).
Reticular hyperpigmentation
Published in Dimitris Rigopoulos, Alexander C. Katoulis, Hyperpigmentation, 2017
Alexander C. Katoulis, Efthymia Soura
DSH is caused by a mutation in the adenosine deaminase, RNA-specific gene (ADAR1). ADAR1 protein is believed to play an important role in several processes, including virus inactivation (e.g., measles virus, HIV, and hepatitis C virus), regulation of innate immune response functions, and alteration of properties of various neurotransmitter receptors.15,23,24 Electron microscopic findings in the hypopigmented areas suggest increased cellular apoptosis, while melanosomes appear to be scattered, smaller than normal, and immature.25 It could be that melanocytes harboring the ADAR1 mutation are more prone to apoptosis when specific stress factors are present (e.g., viral infection).15 This could lead to the initial appearance of the typical hypopigmented lesions.15 However, the exact pathogenetic mechanism of DSH has not been fully elucidated, and it could be considered that other factors besides the ADAR1 mutation may be responsible for the phenotypic appearance of the disorder.25
RNA A-to-I editing, environmental exposure, and human diseases
Published in Critical Reviews in Toxicology, 2021
Here, the RNA sequencing expression data of the tumor and normal samples from the TCGA and GTEx projects were analyzed using a standard processing pipeline. GEPIA was used which is a newly developed interactive web server for analyzing the data from the TCGA and the GTEx projects. It uses RNA sequencing data and makes two datasets compatible (Tang et al. 2017). 18 cancer types among 33 tumor types were chosen and all of them included over 6297 tumors and 4049 normal samples (Table 2). It was observed that ADAR was significantly overexpressed in four cancer types including ESCA, LAML, PAAD, and STAD. Lower expression of ADAR was not observed across cancer types. On the contrary, we observed that ADARB1 and ADARB2 were significantly downregulated in several cancers. For example, ADARB1 was significantly lower expressed in COAD, GBM, KICH, LGG, LUAD, LUSC, and UCEC. Similarly, ADARB2 was significantly lower expressed in COAD, GBM, and TGCT (Figure 1). These findings do not indicate a direct association between A-to-I editing distribution and cancer. However, by altering the A-to-I editing related gene expressions, it could be understood that the level or profiling of RNA editing could change in various cancer types.
Chromosomal 1q21 abnormalities in multiple myeloma: a review of translational, clinical research, and therapeutic strategies
Published in Expert Review of Hematology, 2021
Kamlesh Bisht, Brian Walker, Shaji K. Kumar, Ivan Spicka, Philippe Moreau, Tom Martin, Luciano J. Costa, Joshua Richter, Taro Fukao, Sandrine Macé, Helgi van de Velde
The MM transcriptome is aberrantly hyper edited because of ADAR1 overexpression, conferring enhanced growth and proliferation of MM cells, as well as reduced responsiveness to both standard and novel therapy [124]. Overexpression of ADAR1 is an independent risk factor of poor prognosis [124]. As knockdown of ADAR1 reduces malignant regeneration of high-risk MM in patient-derived xenografts, it is plausible that selective inhibition of ADAR1 may obviate progression and relapse [125] (Figure 3).