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Articles by Miles F. Wilkinson
Nonsense-mediated RNA decay: an emerging modulator of malignancy - Nature Reviews Cancer
Abstract Nonsense-mediated RNA decay (NMD) is a highly conserved RNA turnover pathway that selectively degrades RNAs harbouring truncating mutations that prematurely terminate translation, including nonsense, frameshift and some splice-site mutations. Recent studies show that NMD shapes the mutational landscape of tumours by selecting for mutations that tend to downregulate the expression of tumour suppressor genes but not oncogenes.
Genetic Paradox Explained by Nonsense
AP Photo/Mark Schiefelbein, File Conventional wisdom holds that modifying a gene to make the encoded protein inactive — ‘knocking out' the gene — will have more severe effects than merely reducing the gene's expression level. However, there are many cases in which the opposite occurs. Read Full Article » Related Topics: Genes Show comments Hide Comments Related Articles
Genetic paradox explained by nonsense
NEWS AND VIEWS 03 April 2019 Gene mutations that truncate the encoded protein can trigger the expression of related genes. The discovery of this compensatory response changes how we think about genetic studies in humans and model organisms. Conventional wisdom holds that modifying a gene to make the encoded protein inactive — ‘knocking out’ the gene — will have more severe effects than merely reducing the gene’s expression level. However, there are many cases in which the opposite occurs.
Nonsense-mediated RNA decay in the brain: emerging modulator of neural development and disease
Tarpey, P. S. et al. Mutations in UPF3B, a member of the nonsense-mediated mRNA decay complex, cause syndromic and nonsyndromic mental retardation. Nat. Genet. 39, 1127–1133 (2007). This report is the first to demonstrate that UPF3B mutations are likely to cause ID in humans. The authors also find that patients with ID with UPF3B mutations sometimes have neurodevelopmental disorders, such as schizophrenia. Pilaz, L. et al. Prolonged mitosis of neural progenitors alters cell fate in the developing brain.
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