Results 21 to 30 of about 199,160 (290)
Therapeutic promise of engineered nonsense suppressor tRNAs
Wiley Interdisciplinary Reviews - RNA, 2021 Nonsense mutations change an amino acid codon to a premature termination codon (PTC) generally through a single‐nucleotide substitution. The generation of a PTC results in a defective truncated protein and often in severe forms of disease. Because of the
Joseph J. Porter +2 more
semanticscholar +1 more source
Effect of small molecule eRF3 degraders on premature termination codon readthrough
Nucleic Acids Research, 2021 Premature termination codon (PTC) readthrough is considered a potential treatment for genetic diseases caused by nonsense mutations. High concentrations of aminoglycosides induce low levels of PTC readthrough but also elicit severe toxicity.
Alireza Baradaran-Heravi +5 more
semanticscholar +1 more source
Repurposing tRNAs for nonsense suppression
Nature Communications, 2021 Three stop codons (UAA, UAG and UGA) terminate protein synthesis and are almost exclusively recognized by release factors. Here, we design de novo transfer RNAs (tRNAs) that efficiently decode UGA stop codons in Escherichia coli. The tRNA designs harness
S. Albers +10 more
semanticscholar +1 more source
Biomedicines, 2023 (1) Background: A premature termination codon (PTC) can be induced by a type of point mutation known as a nonsense mutation, which occurs within the coding region. Approximately 3.8% of human cancer patients have nonsense mutations of p53.
Chia-Chi Chen +12 more
doaj +1 more source
Nonsense Codons Trigger an RNA Partitioning Shift [PDF]
Journal of Biological Chemistry, 2009 T-cell receptor-beta (TCRbeta) genes naturally acquire premature termination codons (PTCs) as a result of programmed gene rearrangements. PTC-bearing TCRbeta transcripts are dramatically down-regulated to protect T-cells from the deleterious effects of the truncated proteins that would otherwise be produced.
Miles F. Wilkinson +6 more
openaire +3 more sources
Ataluren—Promising Therapeutic Premature Termination Codon Readthrough Frontrunner
Pharmaceuticals, 2021 Around 12% of hereditary disease-causing mutations are in-frame nonsense mutations. The expression of genes containing nonsense mutations potentially leads to the production of truncated proteins with residual or virtually no function.
Sylwia Michorowska
semanticscholar +1 more source
Transcriptional Silencing of Nonsense Codon-Containing Immunoglobulin Minigenes [PDF]
Molecular Cell, 2005 Cells possess mechanisms to prevent synthesis of potentially deleterious truncated proteins caused by premature translation-termination codons (PTCs). Here, we show that PTCs can induce silencing of transcription of its cognate gene. We demonstrate for immunoglobulin (Ig)-mu minigenes expressed in HeLa cells that this transcriptional silencing is PTC ...
Bühler, Marc +3 more
openaire +3 more sources
A Hox gene mutation that triggers Nonsense-mediated RNA decay and affects alternative splicing during Drosophila development [PDF]
, 2003 Nonsense mutations are usually assumed to affect protein function by generating truncated protein products. Nonetheless, it is now clear that these mutations affect not just protein synthesis but also messenger RNA stability.
Akam, Michael, Alonso, Claudio R
core +2 more sources
BMC Biology, 2009 Background Nonsense-mediated decay is a mechanism that degrades mRNAs with a premature termination codon. That some exons have premature termination codons at fixation is paradoxical: why make a transcript if it is only to be destroyed?
Hu Landian +6 more
doaj +1 more source
Frontiers in Pediatrics, 2022 ObjectiveLiddle syndrome (LS) is a monogenic hypertension consistent with autosomal dominant inheritance, often with early onset high blood pressure in childhood or adolescence.
Di Zhang +11 more
doaj +1 more source