Nonsense-mediated mRNA decay maintains translational fidelity by limiting magnesium uptake
Genes and Development, ISSN: 0890-9369, Vol: 24, Issue: 14, Page: 1491-1495
2010
- 47Citations
- 69Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations47
- Citation Indexes47
- 47
- CrossRef38
- Captures69
- Readers69
- 69
Article Description
Inactivation of the yeast nonsense-mediated mRNA decay (NMD) pathway stabilizes nonsense mRNAs and promotes readthrough of premature translation termination codons. Although the latter phenotype is thought to reflect a direct role of NMD factors in translation termination, its mechanism is unknown. Here we show that the reduced termination efficiency of NMD-deficient cells is attributable to increased expression of the magnesium transporter Alr1p and the resulting effects of elevated Mg levels on termination fidelity. Alr1p levels increase because an upstream ORF in ALR1 mRNA targets the transcript for NMD. Our results demonstrate that NMD, at least in yeast, controls Mg homeostasis and, consequently, translational fidelity. © 2010 by Cold Spring Harbor Laboratory Press.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77954856723&origin=inward; http://dx.doi.org/10.1101/gad.1930710; http://www.ncbi.nlm.nih.gov/pubmed/20634315; http://genesdev.cshlp.org/lookup/doi/10.1101/gad.1930710; https://dx.doi.org/10.1101/gad.1930710; https://genesdev.cshlp.org/content/24/14/1491
Cold Spring Harbor Laboratory
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