Nonsense-mediated mRNA decay in humans at a glance.
Rochester, United States. In J Cell Sci, Feb 2016
In this Cell Science at a Glance and the accompanying poster, we review progress made towards this goal, focusing on human studies and the role of the key NMD factor up-frameshift protein 1 (UPF1).
Insulin Signaling Augments eIF4E-Dependent Nonsense-Mediated mRNA Decay in Mammalian Cells.
Seoul, South Korea. In Biochim Biophys Acta, Jan 2016
We provide evidence that (i) insulin-mediated enhancement of translation augments NMD and rapamycin abrogates this enhancement; (ii) an increase in AKT phosphorylation due to inhibition of PTEN facilitates NMD; (iii) insulin stimulation increases the binding of up-frameshift factor 1 (UPF1), most likely to eIF4E-bound PTC-containing transcripts; and (iv) insulin stimulation induces the colocalization of UPF1 and eIF4E in processing bodies.
Staufen-mediated mRNA decay.
Rochester, United States. In Wiley Interdiscip Rev Rna, 2013
Both STAU1 and STAU2 interact directly with the ATP-dependent RNA helicase UPF1, a key SMD factor, enhancing its helicase activity to promote effective SMD.
UPF1 involvement in nuclear functions.
Birmingham, United Kingdom. In Biochem Soc Trans, 2012
UPF1 (up-frameshift 1) is a protein conserved in all eukaryotes that is necessary for NMD (nonsense-mediated mRNA decay).
Translational control of intron splicing in eukaryotes.
Rouen, France. In Nature, 2008
By knocking down the two P. tetraurelia genes encoding UPF1, a protein that is crucial in NMD, we show that the intrinsic efficiency of splicing varies widely among introns and that NMD activity can significantly reduce the fraction of unspliced mRNAs.