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In addition, we found that the binding is sensitive to imidazole and to pH values of ≤5.8, consistent with an essential role of histidine residues, which are protonated at lower pH and therefore incapable of coordinate bonding with the inhibitor.
These ionic interactions would explain why substrate binding is sensitive to substitutions at these charged positions [e.g., d-Trp, tryptamine, indole priopionic acid, and tryptophanol (Scheme 4)] and in some cases [e.g., tryptamine, indole propionic acid, and tryptophanol (Scheme 4)] essentially eliminates activity altogether.
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CTCF binds to a set of signal sequences, with this binding being sensitive to methylation (Filippova, 2008), while also having the potential to mediate long-range chromosomal interactions (Ling et al., 2006).
In broken cells mitochondrial binding was sensitive to a range of protease treatments.
CDK8 binding was sensitive to IKKβ inhibition and largely unperturbed by Stat1 deficiency.
Indeed, a previous study using the binding task found that the magnitude of binding was sensitive to the strength of the outcome prediction (Moore & Haggard, 2008).
As Asf1 is a histone H3-H4 chaperone, some Asf1 mutants that influence histone binding are sensitive to agents that induce replicative stress or DNA damage [ 23].
We show that both association and dissociation rates of SRP binding are sensitive to active RNC translation, with rapid and stable SRP binding to RNCs only upon exposure of a signal sequence outside the ribosomal peptide tunnel.
In line with these results we could demonstrate that episomal enhancer blocking mediated by a composite binding site is sensitive to a poly(ADP ribosylation inhibitor as well.
With respect to the IRF1 motif, a putative binding site is sensitive to variation at rs6759003 (107 kb from the B3GNT2 transcription stop site), with the risk allele predicted to increase IRF1 affinity (Additional file 16, Part B).
It has been previously demonstrated that FOXP3 binding capability is sensitive to cellular Ca2+ influx and that it can be dramatically increased in T cells upon stimulation with PMA and ionomycin [ 16].
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