Sentence examples for mutant mRNAs containing from inspiring English sources

Nonsense-mediated mRNA Decay (NMD) degrades mutant mRNAs containing premature termination codon (PTC-mRNAs).

In this disease, mutant mRNAs, containing expanded CUG trinucleotide repeats, are thought to interact with key splicing modulators and lead to alternative splicing misregulation.

Previous studies have shown that mutant mRNAs containing the transcribed repeats are retained within the nuclei of DM1 and DM2 cells, where they bind and sequester specific RNA-binding proteins, including Muscleblind-like (MBNL) (Miller et al., 2000).

Previous studies have shown that the mutant mRNAs containing the transcribed CUG or CCUG repeats are retained within the nuclei of cells from individuals with DM, where they bind and sequester the muscleblind-like proteins MBNL1, MBNL2 and MBNL3.

Also, nonsense but not missense mutants of xantha mRNA in barley (Hordeum vulgare) appear to be subjected to rapid degradation, even though the mutant mRNA contains PTC in the last exon [ 53].

This mechanism may also underlie degradation of other mutant SOD1 mRNAs containing a PTC in exons 1 4, the non-terminal exons of SOD1, as NMD appears to be a universal mechanism of the cellular defense against the potentially deleterious effects of truncated proteins (16).

In addition, a minority of the mutant notch3 mRNAs contained aberrantly spliced sequences that result in partial deletions of exon 13.

Quantitative PCR showed that the ratio of the mutant DPD mRNA, containing the 44 bp fragment of intron 10, and wild-type DPD mRNA was 144 ± 6 and 28±13%3% in patient 2 and subject 3, respectively.> -wrap-foot> The mutations indicated in bold were part of a haplotype associated with severe 5FU toxicity (Amstutz et al. 2009) n.a.a

In this disease, the mutant mRNAs (which contain expanded CUG trinucleotide repeats, and are called CUG-RNAs) are thought to interact with, and deregulate, splicing modulators, such as the muscleblind-like protein 1 (MBNL1), driving the main pathogenic effect in DM1.

IGV profiles derived from the mutant strains suggested partial transcriptional readthrough past the normal PCL5 terminator, resulting in 3′-extended mRNAs containing an additional approximately 400 bp on a fraction of the transcripts (red arrow).

Reduction of ribosome recycling in the ΔssrA mutant may only marginally alter the production of efficiently translated, high abundance proteins, while severely impacting the accumulation of low abundance proteins, including regulatory proteins translated from mRNAs containing rare codons, and thereby contribute to the defects we observed.