Sentence examples for binding affinity indicating that from inspiring English sources

Several peptide derivatives, 2, 7 and 8, showed modest but significant binding affinity, indicating that the designed peptide could mimic the VEGF81 91 fragment and therefore disrupt the VEGF/VEGFR-1 interaction.

Moreover, all of these compounds display weak to extremely weak muscarinic receptor binding affinity, indicating that as potential antidepressants, they may overcome certain side effects that are of concern with other antidepressants, which are thought to be mediated by their anticholinergic properties.

On the contrary, 2-butyl-N,N′-bis{[2′-[2H-tetrazol-5-yl)]bromidel-4-yl]methyl}imidazolium bromide (27) (–logIC50 = 5.77) and 2-butyl-4-chloro-5-hydroxymethyl-N,N′-bis{[2′-[2H-tetrazol-5-yl)]biphenyl-4-yl]methyl}imidazolium bromide (30) (–logIC50 = 6.38) displayed very low binding affinity indicating that the orientation of the n-butyl group is of primary importance.

Compared to the high binding affinity of Cl-IB-MECA to the A3 adenosine receptor, the corresponding 3′-fluoro derivative showed remarkably decreased binding affinity, indicating that 3′-hydroxyl group acts as hydrogen bonding acceptor, not hydrogen bonding donor like fluorine atom in binding to the A3 adenosine receptor.

R111A mutant almost completely loses the c-di-GMP binding affinity, indicating that R111 is the most important residue for c-di-GMP binding.

The dimensionless parameter (i.e., ratio of binding affinity) introduced in this work from such experiments is useful in quantitatively depicting such binding affinity, indicating that the binding affinity and stability between AuNPs and catecholamine is approximately 1.5 times stronger than that between amine and AuNPs.

A simple conjugation of a reported collagen-binding sequence and VEGF did not increase the collagen-binding affinity, indicating that the molecular interaction between the two proteins abolished collagen binding activity.

In vitro phosphorylation of MtrA by phosphoramidate caused dimerization of the response regulator and enhanced its DNA-binding affinity, indicating that MtrA is activated by phosphorylation.

Pgamma1-60 binding to the GAF domain increased vardenafil but not cGMP affinity, indicating that substrate- and inhibitor-binding sites do not totally overlap.

Despite the reductions in protease sensitivity, MMP-1 bound to all of the engineered rhCIIIs with comparable affinity, indicating that MMP-1 binding is not sufficient for cleavage.

The increase in binding affinity at lower pH was greater for the Ubx optimal binding site than for other DNA binding sites, indicating that subtle sequence alterations in DNA binding sites may influence pH-dependent behavior.