Sentence examples for antisense guide from inspiring English sources

miRNAs act as antisense guide for the miRISC complex to recognize target protein coding and non-coding RNAs.

In contrast, the antisense (guide) strand that has the complementary sequence to the target mRNA will remain in the RISC and direct recognition and cleavage of the target mRNA.

Toxicity of RNAi can occur through improper target recognition resulting from suboptimal annealing of the antisense guide strand to the target strand, improper selection of an unintended passenger strand by the RISC complex, or overloading of the silencing machinery.

In addition, the seed-region of the siRNA antisense (guide) strand can bind SCRs in the 3′ UTR of mRNA molecules that show only partial complementarity, leading to direct seed-dependent effects.

Membranes were then cross-linked and hybridized with a P end-labelled DNA oligo (5'-End Labelling Kit, GE Healthcare) that detected the antisense guide strand of the miLacZ sequence, in Oligo Hyb Buffer (Ambion) for two days at 36°C.

Complementary oligos were designed and annealed to yield dsDNA inserts with compatible overhangs to BbsI-digested vectors (Cong et al, 2013), the antisense guide was cloned into the spCas9 D10A expressing vector pX335 (Addgene Plasmid #42335) and the sense guide into the puromycin selectable plasmid pBABED P U6 (University of Dundee).

RNAi molecules have sequence complementation to that of the siRNA antisense (or guide) strand ultimately inhibiting the translation of the encoded protein.

Depending on the degree of complementarity between the so-called antisense (or guide) strand of the dsRNA and target mRNA, RNAi can bring about the cleavage of the mRNA (in the case of full or nearly full complementarity), accelerated degradation (as a consequence of deadenylation), or translational repression.

Since forked siRNA duplexes appear to increase the assembly of antisense-strand (guide) siRNA elements into RISCs, the ease of incorporation of antisense-strand siRNA elements into RISCs may be a key factor for improvement of ASP-RNAi activity.

Natural antisense-transcript siRNAs (nat-siRNAs), which derive from pairs of natural-antisense transcripts, guide the cleavage of one of the two parent transcripts, leading to the production of a series of secondary 21-nt siRNAs of unclear function [ 15, 16].

In addition, we also suggest that nucleotide mismatches at the 3'-ends of sense-strand siRNA elements, which possibly increase the assembly of antisense-strand (guide) siRNAs into RNA-induced silencing complexes (RISCs), may enhance ASP-RNAi in the case of inert siRNA duplexes.