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For this, differences were maximized between binding curve kinetic parameters for probes binding to complementary targets versus non-target controls.
They modulate gene function through their binding to complementary regions within the 3'-UTRs of target mRNAs, leading to mRNA degradation or repression of translation.
Although various oligonucleotide backbone modifications have been invented for more efficient binding to complementary RNA [23, 24], these modifications require substitution of multiple nucleotides.
Polyamide nucleic acids (PNAs) are DNA protein chimeric molecules that can be designed with modifications so as to allow good cell entry and high affinity binding to complementary RNA.
They can inhibit the expression of specific messenger RNAs by binding to complementary target sequences located in the 3' untranslated region (3'UTR) [1].
MicroRNAs are small non-coding RNA molecules that regulate mRNA translation and stability by binding to complementary sequences usually within the 3' un-translated region (UTR).
miRNAs have been shown to control mRNA stability and translation by binding to complementary sequence motives in the target mRNAs[6].
Similar(4)
We therefore hypothesized that these were from panel primers promiscuously binding to nearly complementary sequences of nontargeted amplicons.
An antisense drug, designed to look like the original DNA, could interrupt that process by binding to a complementary stretch of RNA and destroying it.
Many of these microRNAs are thought to regulate the translational expression of other genes by binding to partially complementary sites in messenger RNAs.
MicroRNAs (miRNAs) are small noncoding RNAs that modulate gene expression post-transcriptionally by binding to the complementary sequences of targeted mRNAs.
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