Results 31 to 40 of about 418,363 (219)

Noisy splicing, more than expression regulation, explains why some exons are subject to nonsense-mediated mRNA decay

open access: yesBMC 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

A High-Throughput Assay for In Vitro Determination of Release Factor-Dependent Peptide Release from a Pretermination Complex by Fluorescence Anisotropy—Application to Nonsense Suppressor Screening and Mechanistic Studies

open access: yesBiomolecules, 2023
Premature termination codons (PTCs) account for ~12% of all human disease mutations. Translation readthrough-inducing drugs (TRIDs) are prominent among the several therapeutic approaches being used to overcome PTCs.
Mikel D. Ghelfi   +3 more
doaj   +1 more source

A competition between stimulators and antagonists of Upf complex recruitment governs human nonsense-mediated mRNA decay. [PDF]

open access: yesPLoS Biology, 2008
The nonsense-mediated decay (NMD) pathway subjects mRNAs with premature termination codons (PTCs) to rapid decay. The conserved Upf1-3 complex interacts with the eukaryotic translation release factors, eRF3 and eRF1, and triggers NMD when translation ...
Guramrit Singh   +2 more
doaj   +1 more source

2,6-Diaminopurine as a highly potent corrector of UGA nonsense mutations

open access: yesNature Communications, 2020
Nonsense mutations can be corrected by several molecules that activate readthrough of premature termination codon. Here, the authors report that 2,6-diaminopurine efficiently corrects UGA nonsense mutations with no significant toxicity.
Carole Trzaska   +21 more
doaj   +1 more source

A system for coordinated analysis of translational readthrough and nonsense-mediated mRNA decay. [PDF]

open access: yesPLoS ONE, 2017
The nonsense-mediated mRNA decay (NMD) pathway degrades mRNAs containing premature termination codons, limiting the expression of potentially deleterious truncated proteins.
Stacey L Baker, J Robert Hogg
doaj   +1 more source

Statistical analysis of readthrough levels for nonsense mutations in mammalian cells reveals a major determinant of response to gentamicin. [PDF]

open access: yesPLoS Genetics, 2012
The efficiency of translation termination depends on the nature of the stop codon and the surrounding nucleotides. Some molecules, such as aminoglycoside antibiotics (gentamicin), decrease termination efficiency and are currently being evaluated for ...
Célia Floquet   +3 more
doaj   +1 more source

A murine Zic3 transcript with a premature termination codon evades nonsense-mediated decay during axis formation [PDF]

open access: yes, 2016
The ZIC transcription factors are key mediators of embryonic development and ZIC3 is the gene most commonly associated with situs defects (heterotaxy) in humans. Half of patient ZIC3 mutations introduce a premature termination codon (PTC).
Warr, Nicholas   +7 more
core   +1 more source

Translational Attenuation Mechanism of ErmB Induction by Erythromycin Is Dependent on Two Leader Peptides

open access: yesFrontiers in Microbiology, 2021
Ribosome stalling on ermBL at the tenth codon (Asp) is believed to be a major mechanism of ermB induction by erythromycin (Ery). In this study, we demonstrated that the mechanism of ermB induction by Ery depends not only on ermBL expression but also on ...
Shasha Wang   +8 more
doaj   +1 more source

2A peptides provide distinct solutions to driving stop-carry on translational recoding [PDF]

open access: yes, 2011
Funded by the U.K. Biotechnology and Biological Sciences Research Council (BB/E/01070911)Expression of viral proteins frequently includes non-canonical decoding events (‘recoding’) during translation. ‘2A’ oligopeptides drive one such event, termed ‘stop-
Yan, F   +16 more
core   +1 more source

UPF1 silenced cellular model systems for screening of read-through agents active on β039 thalassemia point mutation

open access: yesBMC Biotechnology, 2018
Background Nonsense mutations promote premature translational termination, introducing stop codons within the coding region of mRNAs and causing inherited diseases, including thalassemia.
Francesca Salvatori   +7 more
doaj   +1 more source

Home - About - Disclaimer - Privacy