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| http://dx.doi.org/10.1073/pnas.0901936106 | DOI Listing |
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The transcriptional and translational landscape of HCoV-OC43 infection.
PLoS Pathog
January 2025
Discovery Research Platform for Hidden Cell Biology, University of Edinburgh, Edinburgh, Scotland, UK.
The coronavirus HCoV-OC43 circulates continuously in the human population and is a frequent cause of the common cold. Here, we generated a high-resolution atlas of the transcriptional and translational landscape of OC43 during a time course following infection of human lung fibroblasts. Using ribosome profiling, we quantified the relative expression of the canonical open reading frames (ORFs) and identified previously unannotated ORFs.
View Article and Find Full Text PDFThe SARS-CoV-2 nucleocapsid protein interferes with the full enzymatic activation of UPF1 and its interaction with UPF2.
Nucleic Acids Res
January 2025
Molecular Microbiology and Structural Biochemistry, MMSB-IBCP, CNRS UMR 5086 , Université Claude Bernard Lyon 1, F-69367 Lyon, France.
The nonsense-mediated mRNA decay (NMD) pathway triggers the degradation of defective mRNAs and governs the expression of mRNAs with specific characteristics. Current understanding indicates that NMD is often significantly suppressed during viral infections to protect the viral genome. In numerous viruses, this inhibition is achieved through direct or indirect interference with the RNA helicase UPF1, thereby promoting viral replication and enhancing pathogenesis.
View Article and Find Full Text PDFWhen "loss-of-function" means proteostasis burden: Thinking again about coding DNA variants.
Am J Hum Genet
January 2025
Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
Each human genome has approximately 5 million DNA variants. Even for complete loss-of-function variants causing inherited, monogenic diseases, current understanding based on gene-specific molecular function does not adequately predict variability observed between people with identical mutations or fluctuating disease trajectories. We present a parallel paradigm for loss-of-function variants based on broader consequences to the cell when aberrant polypeptide chains of amino acids are translated from mutant RNA to generate mutated proteins.
View Article and Find Full Text PDFEngineered tRNAs efficiently suppress CDKL5 premature termination codons.
Sci Rep
December 2024
Department of Medical Biotechnology and Translational Medicine, University of Milan, Segrate (Milan), 20054, Italy.
Article Synopsis
- The CDKL5 deficiency disorder (CDD) is a severe neurodevelopmental condition with symptoms including early epilepsy, intellectual disabilities, and motor/visual dysfunction, caused by mutations in the CDKL5 gene.
- Currently, there is no cure for CDD; treatments focus on managing seizures, though some genetic therapies show promise in addressing the disorder's root causes.
- Recent studies using Anticodon-edited tRNAs (ACE-tRNAs) have shown potential in restoring full-length CDKL5 protein synthesis, opening up possibilities for effective new treatments for patients with nonsense mutations.
Optimization of ACE-tRNAs function in translation for suppression of nonsense mutations.
Nucleic Acids Res
December 2024
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave., Rochester, NY 14642, USA.
Nonsense suppressor transfer RNAs (tRNAs) or AntiCodon-Edited tRNAs (ACE-tRNAs) have long been envisioned as a therapeutic approach to overcome genetic diseases resulting from the introduction of premature termination codons (PTCs). The ACE-tRNA approach for the rescue of PTCs has been hampered by ineffective delivery through available modalities for gene therapy. Here we have screened a series of ACE-tRNA expression cassette sequence libraries containing >1800 members in an effort to optimize ACE-tRNA function and provide a roadmap for optimization in the future.
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