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Genetics
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
RNA translation to protein (cytoplasm)Mediated by transfer RNAs (tRNAs).mRNA are ‘coding’ RNAs – translated into proteins.microRNA are ‘non-coding’ RNAs– not translated → modulate protein expression by annealing to mRNA:The 5' end of miRNA binds to the 3' end of mRNA.miRNA‒mRNA pair recruits a silencing complex: RNA induced silencing complex (RISC) → the fate of mRNA depends on the complementation.‘Perfect complementation’→ mRNA degradation.‘Imperfect complementation’ → altered translation of mRNA (may lead to oncogenesis).
Introduction to virus structure, classification, replication, and hosts
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Philippe Simon, Kevin M. Coombs
The greatest variability among viral life cycles occurs during the middle stage. As indicated earlier, events that take place during this time are transcription (the process whereby the nucleic acid, whether RNA or DNA, is copied to produce complementary positive-sense mRNA), translation (“reading” of the mRNA nucleotide sequence by cellular ribosomes to produce a corresponding order of linked amino acids that form a polypeptide protein) and replication (the copying of parental genomic material that serves as the template to produce an identical copy).
Replication
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
As it follows from Chapters 13 and 16, the specific RNA synthesis process is tightly coupled with the phage RNA translation, and the whole replication cycle is fully subjected to the translational control. First, both replication and translation share common interchangeable components, namely, the ribosomal protein S1, the elongation factors EF-Tu and EF-Ts, and the Hfq chaperone. Second, RNA replication occurs simultaneously with RNA translation on the nascent RNA plus strand chains. Third, the parameters of the whole replication cycle are determined by special regulatory mechanisms, namely, the polarity phenomenon and the controlling action of the two repressor complexes I and II that were described in Chapter 16.
The molecular structure and biological functions of RNA methylation, with special emphasis on the roles of RNA methylation in autoimmune diseases
Published in Critical Reviews in Clinical Laboratory Sciences, 2022
Wanwan Zhou, Xiao Wang, Jun Chang, Chenglong Cheng, Chenggui Miao
N1-methyladenosine (m1A), N6,2-O-dimethyladenosine (m6Am), and 7-methylguanosine (m7G) are newly discovered types of RNA methylation. The m1A modification is abundant in post-transcription transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs) in eukaryotes and affects the regulation of mRNA translation [21]. The m6Am modification is an evolutionarily conserved change that differs functionally from m6A, does not alter mRNA transcription or stability, but negatively affects the cap-dependent translation of methylated mRNAs [22]. The m7G modification regulates mRNA transcription, microRNA (miRNA) biosynthesis, biological functions, tRNA stability, 18S rRNA processing, and maturation [23]. The relationships between m1A, m6Am, and m7G modifications and autoimmune diseases have not been reported and their functions and mechanisms need to be explored.
ELX-02: an investigational read-through agent for the treatment of nonsense mutation-related genetic disease
Published in Expert Opinion on Investigational Drugs, 2020
Nonsense mutations are single nucleotide changes in the coding region of a DNA sequence that introduces an early (or premature) stop codon [1]. During mRNA translation, the ribosome pauses upon reaching the stop codon introduced by the nonsense mutation, which then allows termination factors to bind and signal the premature end of protein synthesis Figure 1 [2]. The resulting truncated protein products may be unstable or lack critical domains such as localization signals, which in either case results in a loss of protein function [3]. In addition to interrupting protein translation, a proof-reading mechanism known as nonsense-mediated mRNA decay (NMD) targets transcripts bearing some nonsense mutations for degradation [4]. The reduced mRNA stability resulting from NMD may reduce the steady-state expression level. Therefore, single nucleotide changes can reduce both mRNA and protein levels of essential genes. Globally, nonsense mutations account for ~11% of all described gene lesions causing inherited monogenetic diseases [1], most of which have few or no available disease-modifying therapies.
The MAP kinase-interacting kinases (MNKs) as targets in oncology
Published in Expert Opinion on Therapeutic Targets, 2019
Jianling Xie, James E. Merrett, Kirk B. Jensen, Christopher G. Proud
Regulating gene expression is critical for the normal functioning of cells by allowing them to adapt to changes in their intra- and extra-cellular environments, respond to growth stimuli, hormones, cytokines and manage various stresses. Dysregulated gene expression can lead to abnormal cell growth and transformation [6]. mRNA translation is a key site for regulating gene expression and major signalling pathways converge upon it, particularly on the initiation of translation, where most control over mRNA translation is exerted [7]. Major signalling pathways that regulate translation initiation include the mammalian target of rapamycin complex (mTORC1) and mitogen-activated protein kinase (MAPK) pathways, which are activated by hormones and growth factors and by oncogenic signalling proteins (such as Kras[G12V]) or loss of tumour suppressors, e.g., PTEN (phosphatase-and-tensin homologue).