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Individual miRNAs can affect many target genes, silencing their expression either by preventing translation of the intermediate molecules (i.e., messenger RNAs [mRNAs]) that are generated during transcription or by causing mRNA cleavage.
MicroRNAs (miRNAs) are small, noncoding RNAs that negatively regulate gene expression by preventing translation of specific mRNA transcripts and are known to play a role in many cancers (including oral) [ 2, 3].
These results show that the presence of the Hes5-1 3'UTR in the pCAG-VNP vector strongly reduces the levels of reporter expression, most likely by decreasing the half-life of the VNP mRNA or by preventing translation of the reporter protein.
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MiRNAs are small, 19-23 nucleotide, non-coding RNAs that repress the expression of target genes by either preventing translation of the target mRNA or causing its degradation.
Other AO-induced mechanisms of gene downregulation may involve the steric inhibition of ribosomal complex formation by preventing translation initiation, modulating the pre-mRNA splicing process to disrupt the reading frame or by removing exons encoding crucial functional domains [20].
MicroRNAs (miRNAs) are responsible for specific down-regulation of gene expression at a post-transcriptional level, by preventing translation from messenger RNAs.
Hence, even though we observe an increase in PDK4 mRNA expression (Figure 3A), post-transcriptional inhibition by miR-107 prevents translation of PDK4 mRNA thus preventing an increase in PDK4 protein content (Figure 3B).
The location of the asRNA transcript suggests it may function to prevent translation of Mb1618c mRNA by steric hindrance of the ribosome binding site.
CsrA can bind to this structure and prevent translation of the lysis protein by obscuring the Shine-Dalgarno sequence (SD) and preventing ribosomal binding.
This growth arrest can be rescued by exogenous expression of the fusion and a mutant designed to prevent translation of the ELK4 protein.
While experimental bone regeneration approaches commonly employ cells, technological hurdles prevent translation of these therapies.
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