Table 1 shows that both indomethacin and CF3 indomethacin are unable to inhibit an Arg-120 to Ala mutant or a Tyr355 to Phe mutant of COX-2, suggesting that the carboxylate of each inhibitor interacts with those residues at the constriction site.
At a 100-fold higher concentration (1.3 µm), PF-879 inhibited GDF-11-mediated activity by 30%, and was unable to inhibit either activin A- or B-induced activity.
Both NAC and DEX were unable to inhibit TNFα induction of either Rel A or p50.
Glyma14g04260's second domain and both domains of Glyma14g04291 were further unable to inhibit cathepsin-B, even at a concentration of 1 mM (Table 1).> -wrap-foot> *a (4 weeks – 8 weeks); *b (8 weeks – 14 weeks); *c (4 weeks −14 weeks); NI represents inhibition ≥20%; *significant at p ≤0.05.
Further, Glyma15g36180 inhibited cathepsin-L, but was unable to inhibit cathepsin-B, even when an inhibitor concentration of 1 mM was used.
Finally, it is important to underline that control experiments demonstrated that AP5 did not have any effect on the catalytic activity of factor Xa, since high concentrations of peptide were unable to inhibit factor Xa activity toward both a chromogenic substrate and prothrombin (data not shown).
If children increased performance but kept making mistakes, this is likely due to motor inhibition problems: being unable to inhibit the prepotent direct-reaching response.
Figure 1B shows that this mutant did not have a DN phenotype, since it was unable to inhibit the toxicity of the wildtype toxin when used a sub-stoichiometric or equimolar ratios.
The latter was unable to inhibit pAKT, and pHER2 was affected only to a limited extent; thus, the inhibition of SP was moderate, as seen for the MAPK inhibitor AG1478 signalling through pMAPK (Supplementary Figure S4).
MvCsk was unable to inhibit MvSrc; treatment with MvCsk actually caused a slight increase in MvSrc activity, perhaps because of the disruption of an autoinhibitory interaction.
