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We hypothesized that polymorphisms in microRNA (miRNA) response elements (MRE-SNPs) that either disrupt a miRNA binding site or create a new miRNA binding site can affect the allele-specific expression of target genes.
Other than SNPs within miRNA target sites, SNPs outside miRNA binding site can affect miRNA function.
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Differential methylation at CTCF-binding sites can affect the imprinted expression of the genes regulated by the insulators, e.g., H19.
Response elements for the two agonists are different, such that a mutation in one site can affect binding of one agonist without affecting the other (Chakrabarty et al, 2005).
It has been believed that allostery refers to the situations where the binding of a ligand to one site can affect the other through a propagated change in the protein shape.
However, one issue needs to be highlighted in this regard – mutations far away from the binding site can potentially affect the shape and or binding affinity of the binding pocket.
Phosphorylation of the first and second Akt phosphorylation sites can affect DNA binding and regulate transcriptional activity of Foxos [43] [43] [43] [43].
SNPs in miRNA target sites can affect miRNA binding to the target mRNA and subsequent gene regulation (Borel and Antonarakis, 2008; Gamazon et al., 2012; Ryan et al., 2010; Saetrom et al., 2009).
Mutational deletion of HA glycosylation sites can affect viral receptor binding [30].
Formation of the composite sites can affect also in vivo binding specificity, and this has been demonstrated in the case of ETS1/RUNX1 (Hollenhorst et al, 2009).
Instead, we found that the half-life and topology of interactions that each condensin binding site can engage in profoundly affects chromosome behavior.
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