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Recent studies have shown that transposons also contribute to the evolution of miRNA genes, products of which are approximately 21-nt small RNAs that can mediate sequence-specific regulation of endogenous gene expressions by binding to complementary sites on target mRNAs [11], [12].
Plant miRNAs negatively regulate their cognate mRNAs by fully or partly binding to complementary sites.
Several evidences have shown that most plant miRNAs function by either perfectly or near-perfectly binding to complementary sites on their target mRNA sequences [ 52].
MicroRNAs (miRNAs) are highly conserved, small, noncoding RNAs that regulate gene expression by binding to complementary sites on target transcripts and are important modulators of pathophysiology processes.
They cause posttranslational gene expression silencing by binding to complementary sites on their target mRNAs and initiate either degradation or inhibition of translation.
The miRNAs play an important role in regulating gene expression at the posttranscriptional level by binding to complementary sites on target mRNAs that either block mRNA translation or trigger mRNA degradation.
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The average predicted free energy of binding for the modified library to complementary sites on the wild-type RNA is −9.2 ± 0.8 kcal/mol at 37 °C, compared with −2.4 ± 1.6 kcal/mol for an unmodified DNA library.
MicroRNAs (miRs) have been shown to negatively regulate gene expression by binding to complementary sequence sites in the 3′-untranslated regions of the mRNAs of protein-coding genes, thereby degrading or blocking the translation of these mRNAs.
Many of these microRNAs are thought to regulate the translational expression of other genes by binding to partially complementary sites in messenger RNAs.
We know that miRNA can act by binding to the complementary sites on the 3′ untranslated region (UTR) of the target gene to induce cleavage with near perfect complementarity or to repress productive translation [ 21].
MicroRNAs exert transcriptional/post transcriptional gene expression regulation through binding to partially complementary sites in the 3″-untranslated region of target genes.
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