Sentence examples for binding to these mutants from inspiring English sources

The effect of bevirimat binding to these mutants likely promoted, rather than disrupted, virion maturation.

As a result, the values of kon and koff for rGTP binding to these mutants were determined from the data (Table 1).

PEPD-induced ErbB2 phosphorylation at both pY1221/1222 and pY1196 in both ErbB2/delD1 and ErbB2/delD2 was comparable to that in WT-ErbB2, absent in ErbB2/delD3 and attenuated in ErbB2/delD4, which correlated well with PEPD binding to these mutants.

There are significant quantitative differences observed between the inhibitors upon binding to these mutant NAs.

The intensity of binding to these was enhanced with mutant viruses (D222G mutation of hemagglutinin) isolated from cases of severe or fatal pdm virus infection: with the D222G mutant pdm viruses there was binding also to nonsulfated internally fucosylated (VIM-2 antigen-bearing) sequences of the type expressed on ciliated cells of the bronchus (Fig. 6).

Affinity and specificity of TxA2 binding to the mutant receptor were identical to wild type receptors.

Similar results are also observed for ubiquitin, although reactions are less efficient, consistent with the weaker noncovalent binding of ubiquitin to these mutants.

To test the binding of these mutants to β-catenin in vivo, we introduced them into full-length FLAG-tagged BCL9, and also generated the corresponding mutants in BCL9-2 (L408FigL411K; Fig. 1A), and co-expressed these with HA-tagged β-catenin in HEK 293T cells.

Lastly, in order to quantitatively compare the binding of these mutants to the 60S subunit, we measured the affinities of these mutants to the 60S subunit using Bio-layer interferometry (BLI) (Figs. 3E and S2).

These effects correspond with the decrease in binding affinity of AM to these mutants at the AM1 receptor ECD, as determined using surface plasmon resonance (Kusano et al., 2012).

The binding of these mutants to the Pikp-HMA was tested in yeast and in vitro.