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These small (∼21-mer) non-coding RNA molecules regulate gene expression by binding to 3' untranslated regions (3' UTR) of target mRNAs, triggering transcript degradation or translational repression depending on the extent of complementarity between the seed sequence of the miRNA and the mRNA motif [3].
The first important step is to identify the extent of complementarity, because it is a prerequisite for synergy to happen (Fig. 4).
This study presents a detailed picture of European Union (EU) and EU member state originating DAH between 2006 and 2009; with a specific focus on assessing the extent of complementarity of development assistance sourced from the EU.
The time point for maximum target gene suppression generally varies depending on the number of miRNA binding sites at the 3′ UTR of the target gene and the extent of complementarity of the seed region [ 37].
The different levels of transcripts (see Table 4) should be discussed by taking in consideration the hierarchy of splicing events associated with the differential extent of complementarity with U1 and U6 small nuclear RNAs (snRNAs), as suggested by Roca et al. (see also Figure 9 and Table 5) [ 42].
The issue of the different ratios of the transcripts corresponding to the 115, 137, 153, and 165 bp amplicons in the cellular systems considered (see Table 4) should be discussed by taking in consideration the hierarchy of splicing events associated with the differential extent of complementarity with U1 and U6 small nuclear RNAs (snRNAs), as suggested by Roca et al. (see Table 5) [ 42].
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This complex either directs the cleavage of complementary target mRNAs [ 2, 3, 6] or inhibits their translation [ 7] primarily depending on the extent of sequence complementarity between the miRNA and the target mRNA.
In addition, the intracellular localization of virus/host mRNAs and miRNAs, the extent of base pairing complementarity of the competitive RNAs, as well as the time-course of viral RNA expression may also impact ceRNA networks.
The mature miRNA guides the miRISC to target mRNAs through base-pairing and directs posttranscriptional repression, the mechanism of which is largely dependent on the extent of base-pairing complementarity between the two nucleic acids.
To measure the extent of the dual complementarity (DC), we counted the number of tRNA pairs with complementary anticodons in which the second bases of the acceptor helix were also complementary, and divided it by the total number of pairs [ 22].
miRNAs can induce translational repression of a target transcript and/or mRNA degradation depending to some extent on the degree of complementarity between the miRNA and binding sites in the 3' untranslated regions (3'UTR) of its target [ 1- 3].
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