Results 11 to 20 of about 59,267 (253)

Unraveling the influences of sequence and position on yeast uORF activity using massively parallel reporter systems and machine learning

open access: yeseLife, 2023
Upstream open-reading frames (uORFs) are potent cis-acting regulators of mRNA translation and nonsense-mediated decay (NMD). While both AUG- and non-AUG initiated uORFs are ubiquitous in ribosome profiling studies, few uORFs have been experimentally ...
Gemma E May   +5 more
doaj   +1 more source

MARVELD1 Inhibits Nonsense-Mediated RNA Decay by Repressing Serine Phosphorylation of UPF1. [PDF]

open access: yesPLoS ONE, 2013
We have observed low expression levels of MARVELD1, a novel tumor repressor, in multiple tumors; however, its function in normal cells has not been explored.
Jianran Hu, Yu Li, Ping Li
doaj   +1 more source

Attenuation of nonsense-mediated mRNA decay enhances in vivo nonsense suppression. [PDF]

open access: yesPLoS ONE, 2013
Nonsense suppression therapy is an approach to treat genetic diseases caused by nonsense mutations. This therapeutic strategy pharmacologically suppresses translation termination at Premature Termination Codons (PTCs) in order to restore expression of ...
Kim M Keeling   +10 more
doaj   +1 more source

Cryo-EM reconstructions of inhibitor-bound SMG1 kinase reveal an autoinhibitory state dependent on SMG8

open access: yeseLife, 2021
The PI3K-related kinase (PIKK) SMG1 monitors the progression of metazoan nonsense-mediated mRNA decay (NMD) by phosphorylating the RNA helicase UPF1. Previous work has shown that the activity of SMG1 is impaired by small molecule inhibitors, is reduced ...
Lukas M Langer   +3 more
doaj   +1 more source

When a ribosome encounters a premature termination codon [PDF]

open access: yesBMB Reports, 2013
In mammalian cells, aberrant transcripts harboring a prematuretermination codon (PTC) can be generated by abnormal orinefficient biogenesis of mRNAs or by somatic mutation.Truncated polypeptides synthesized from these aberranttranscripts could be toxic ...
Jungwook Hwang, Yoon Ki Kim
doaj   +1 more source

Boundary‐independent polar nonsense‐mediated decay [PDF]

open access: yesEMBO reports, 2002
Nonsense‐mediated decay (NMD) is an RNA surveillance mechanism that degrades mRNAs containing premature termination (nonsense) codons. The second signal for this pathway in mammalian cells is an intron that must be at least ∼55 nucleotides downstream of the nonsense codon.
Jun, Wang   +3 more
openaire   +2 more sources

Viral subversion of nonsense-mediated mRNA decay [PDF]

open access: yesRNA, 2020
Viruses have evolved in tandem with the organisms that they infect. Afflictions of the plant and animal kingdoms with viral infections have forced the host organism to evolve new or exploit existing systems to develop the countermeasures needed to offset viral insults.
Maximilian Wei-Lin Popp   +2 more
openaire   +2 more sources

Nonsense-mediated mRNA decay in mammals [PDF]

open access: yesJournal of Cell Science, 2005
Nonsense-mediated mRNA decay (NMD) in mammalian cells generally degrades mRNAs that terminate translation more than 50-55 nucleotides upstream of a splicing-generated exon-exon junction (reviewed in [Maquat, 2004a][1]; [Nagy and Maquat, 1998][2]).
openaire   +4 more sources

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

Nonsense mutations in alpha-II spectrin in three families with juvenile onset hereditary motor neuropathy [PDF]

open access: yes, 2019
Distal hereditary motor neuropathies are a rare subgroup of inherited peripheral neuropathies hallmarked by a length-dependent axonal degeneration of lower motor neurons without significant involvement of sensory neurons.
Asselbergh, B   +10 more
core   +1 more source

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