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Biology of Coronaviruses and Predicted Origin of SARS-CoV-2
Published in Debmalya Barh, Kenneth Lundstrom, COVID-19, 2022
Giorgio Palù, Alberto Reale, Nicolas G. Bazan, Pritam Kumar Panda, Vladimir N. Uversky, Murat Seyran, Alaa A. A. Aljabali, Samendra P. Sherchan, Gajendra Kumar Azad, Wagner Baetas-da-Cruz, Parise Adadi, Murtaza M. Tambuwala, Bruce D. Uhal, Kazuo Takayama, Ángel Serrano-Aroca, Tarek Mohamed Abd El-Aziz, Adam M. Brufsky, Kenneth Lundstrom
The SARS-CoV-2 genome showed approximately 88% similarity to those of two bat viruses, bat-SL-CoVZC45 and bat-SL-CoVXC21, but it was much lower for the SARS-CoV (79%) and the MERS-CoV (50%), respectively [29]. CoVs have three main structural proteins: a very large (200 kDa) S glycoprotein (spike) forming the bulky (15–20 nm) peplomer on the virus surface, an irregular transmembrane glycoprotein (M) and an internal, phosphorylated nucleocapsid protein (N). There is also a small transmembrane envelope protein (E), and a few members of the CoV family contain a further envelope protein with both esterase and hemagglutinin functions. The approximately 30 kb genome of CoVs is a non-segmented, single-stranded RNA (ssRNA) molecule with a positive-sense polarity [30] with a capped 5′ end and polyadenylated 3′-end. As a consequence of heterologous RNA recombination, extensive rearrangements can occur. At the 5′ end of the genome is located an untranslated region (UTR) of 65–98 nucleotides. The 3′ end of the RNA genome contains a poly (A) tail with another UTR sequence of 200–500 nucleotides. For the regulation of RNA replication and transcription, both UTRs are essential [31].
Nucleic Acids as Therapeutic Targets and Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Usually 25 bases in length, Morpholinos bind to complementary sequences of RNA by standard nucleic acid base pairing. They do not degrade their target RNA molecules, unlike many antisense structural types (e.g., phosphorothioates, siRNA). Instead, they act by binding to a target RNA sequence and causing a steric block to transcription. In particular, bound to the 5′-untranslated region of messenger RNA (mRNA), they can interfere with the progression of the ribosomal initiation complex from the 5′-cap to the start codon. This prevents translation of the coding region of the targeted transcript.
Exercise-Induced Mitochondrial Biogenesis: Molecular Regulation, Impact of Training, and Influence on Exercise Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Hashim Islam, Jacob T. Bonafiglia, Cesare Granata, Brendon J. Gurd
The stability of newly transcribed mRNAs is dependent on their interaction with various RNA-binding proteins that either destabilize or stabilize the transcript via binding to specific structural elements of the mRNA (e.g., poly-[A] tail, 3’ untranslated region) (51). Although changes in gene expression are frequently attributed to enhanced mRNA synthesis (i.e., transcription), early experiments revealed an important role for mRNA stability in the initial adaptive response to contractile activity (27). For instance, increases in cytochrome c mRNA expression in electrically stimulated rat skeletal muscle are primarily attributed to the increase in mRNA stability (2–4 days) that precedes the increase in cytochrome c transcription observed after 5 days of stimulation (27). Additionally, the mRNA decay rates of key mitochondrial biogenic regulators (e.g., PGC-1a, TFAM) appear to be accelerated in contracted rat skeletal muscle; this response has been hypothesized to contribute to enhanced turnover of regulatory protein to facilitate a rapid adaptive response to environmental stress (68). Together, these observations highlight the importance of mRNA stability as an important and modifiable regulatory step in the regulation of mitochondrial phenotype, warranting future research in this area (particularly in humans).
Identification of a Novel Mutation in the 3′ Untranslated Region of the β-Globin Gene (HBB:c.*132C>G) in a Chinese Family
Published in Hemoglobin, 2022
Yun-Jing Wen, Qiu-Xia Yu, Fan Jiang, Dong-Zhi Li
β-thalassemia (β-thal) is caused by genetic mutations in the HBB gene which causes a reduced β-globin chain production of hemoglobin. There are more than 200 mutations associated with β-thal (https://globin.bx.psu.edu), and the spectrum and frequency of mutations varies significantly in different regions of the world. Mutation type is a major determinant of clinical phenotype in β-thal. Most of the mutations involve a change within the exons or at the splice junctions that abolish the HBB function with no β-globin production (β0-thal). Other mutations involve noncoding regions such as the promoter region, the 5′ or 3′-untranslated regions (UTRs), introns, and some splicing abnormalities, only compromise HBB function that results in a decrease in β-globin production with mild or silent phenotype (β+ or β++-thal) [1,2]. In this study, we report a novel 3′-UTR mutation, HBB:c.*132C>G, which led to β-thal intermedia (β-TI) in a patient when combined with a β0-thal mutation.
In vivo and in vitro impact of miRNA-153 on the suppression of cell growth apoptosis through mTORC2 signaling pathway in breast cancer
Published in Journal of Receptors and Signal Transduction, 2022
Haimei Liu, Hongyan Zang, Jilin Kong, Liguo Gong
The miRNAs are short non-coding RNA molecules, which could regulate post-transcriptional gene modifications and mediate various pathophysiological processes [8,9]. The miRNAs inhibit mRNA translation or reduce mRNA stability by binding to 3′ untranslated region (3′ UTR) of target mRNA and thereby impact the functionally diversity of gene expression [10,11]. Researches show that abnormal expression of certain miRNA could regulate cell apoptosis, proliferation, angiogenesis and invasion in malignant tumor [12–14]. The miRNA-153 as an ancient and conserved miRNA, which was associated with tumor development and provided cancer targeted therapy a promising research direction [15–17]. The role of miRNA-153 (miR-153) in breast cancer has been investigated in several studies [18–20]. Recently, miRNA-153 was revealed to be involved in the development and progression of breast cancer [21–23]. miRNA-153 could inhibit breast cancer cell proliferation, migration, invasion [24]. Furthermore, MiRNA-153 was demonstrated to promotes breast cancer cell apoptosis and miRNA-153 silencing induces apoptosis in the MDA-MB-231 breast cancer cell line [25,26]. Together, these results suggest that miRNA-153 may serve a tumor-suppressive role in breast cancer.
β-Thalassemia Intermedia Caused by the β-Globin Gene 3′ Untranslated Region: Another Case Report
Published in Hemoglobin, 2022
Fan Jiang, Gui-Lan Chen, Jian Li, Xue-Wei Tang, Dong-Zhi Li
β-Thalassemia (β-thal) is characterized by the absence or reduction of β-globin synthesis. Mutations that entirely silence the β gene expression with no β-globin production result in β0-thal. Others only partly compromise the production of β-globin, with some degree of output of the β chains, causing β+- or β++-(silent) thal. Although most of the molecular lesions involve the structural β gene directly, some downregulate the gene through disturbing RNA processing [1]. The 3′ untranslated region (3′UTR) is associated with mRNA stability because of its involvement in 3′ end processing, polyadenylation, and mRNA capping. Mutations located in this area have been reported to cause a phenotype compatible with β+-thal [2]. We here report a Chinese family with another case of a 3′UTR mutation causing severe β-thal syndrome when combined with a β0-thal.