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It remains to be established whether miRNA/RISC also suppresses translational initiation by causing the mRNA to exit translation, by recruiting the mRNA to P-bodies, or by promoting the association of RBPs that transport the mRNA to P-bodies [19].
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RNA interference (RNAi) is a biological process in which RNA molecules inhibit gene expression, typically by causing the destruction of specific mRNA molecules.
Much evidence shows that mammalian miRNAs, like their plant counterparts, can influence gene expression not only by inhibiting protein translation, but also by causing the degradation of their target mRNA [14] [16].
A shortcoming in this design is that the processing of primary miRNA (pri-miRNA) by Drosha will cause the mRNA to lose their 3' polyadenylation, which destabilizes the mRNA and reduces levels of the reporter gene expression.
This suggests that excess Dhh1 may promote the quick transition of mRNA through P-bodies in order to accumulate in stress granules, or may cause the mRNA to by-pass P-bodies and directly accumulate in stress granules from the translating pool.
miRNAs control gene expression at the posttranscriptional level by causing mRNA degradation and/or repressing mRNA translation.
This complex regulates translation by binding to 3′ regions of untranslated mRNAs by directly inhibiting mRNA translation or by causing mRNA degradation (depending on the degree of complementarity between the miR and the mRNA target).
Thus we suggest that the interaction between influenza RNA polymerase and cellular phosphorylated-RNA polymerase II might be promoted by highly temperature thereby causing the increased mRNA levels.
The cop1 4 mutant causes CO mRNA to accumulate earlier under SDs, so that cop1 4 mutations may in part accelerate flowering under SDs by causing CO mRNA to be expressed in the light, as previously shown for toc1-1 mutants (Yanovsky and Kay, 2002).
miRNAs negatively regulate the expression of their target genes by causing translational arrest, mRNA cleavage or a combination of the two, mostly via direct targeting of the 3′-UTRs of mRNAs.
MiRs bind to the 3'-untranslated region (UTR) of target mRNAs and inhibit their expression by causing mRNA cleavage or inhibition of translation.
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