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Virus-host interactions start with binding of the envelope protein E to a cellular receptor.
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The centromeric nucleosome is then re-established in a step-wise process, most likely starting with binding of CBF1 to CDEI, and CBF3 to CDEIII with assistance of Scm3 (Camahort et al., 2007; Mizuguchi et al., 2007).
Most studies in this field deal with regulatory SNPs in binding sites of TATA-binding protein (TBP) in the region [-70; -20] upstream of the transcription start of various mRNAs encoded in the human genome [ 72, 73] (assembly of the preinitiation complex starts with binding of RNA polymerase to the anchoring TBP/DNA complex [ 74, 75]).
The cyclization reaction starts with binding of a linear saccharide chain across the nine sugar binding subsites labelled −7 to +2 (Fig. 1; Strokopytov et al. 1996), with glycosidic bond cleavage occurring between the −1 and +1 subsites, to yield a stable covalent glycosyl enzyme intermediate (Uitdehaag et al. 1999b).
We have explored two aspects of the pathway: 1) the cascade of signaling events starting with binding of adrenaline to its receptor and ending with the activation of glycogen phosphorylase (tests 1 and 3); and 2) a more focused aspect, the regulation of activation of protein kinase A (PKA; test 2).
Pathogen recognition and attachment onto host cells often starts with the binding of glycan binding proteins (GBPs) to glycan receptors on the host cell surface.
Thus, one can conclude that after the injection of the precursor CdCl2 into the water solution of polymer the formation of NPs seeds starts with the binding of Cd2+ ions with macromolecules via the formation of the coordination compound metal-polymer.
The ThDP-catalyzed carboligation of aldehydes involves a multistep mechanism, which starts with the binding of the donor aldehyde to the ThDP-ylide resulting in an umpolung of the carbonyl reactivity yielding a so-called "activated aldehyde" (for details see the Supporting Information, Figure S1).
Rho-dependent termination starts with the binding of Rho to the RNA at a Rho utilization (rut) site, which is a C-rich region of 85 97 nt.
To start with, CTCF binding sites are known to be flanked by an array of phased nucleosomes.
We suggest that binding starts with a transient binding of AR-C155858 that involves residues toward the cytoplasmic side of MCT1 and that this is required to 'shuttle' the inhibitor to the final site indicated in Figure 7.
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