The illustration of the predicted binding model and the binding sites between celastrol and proteasome β1 subunit are shown in Figures 2b and c, respectively.
Our calorimetric data were fitted to a sequential binding model, and the thermodynamic parameters for the binding of GlcNAc to AAL-2 are summarized in Table 1.
This continuous distribution model has been widely used for MIPs since it can give an adequate approximation of the broad unimodal distribution compared to discrete binding models and the binding site heterogeneity can be quantified.
The superset of data collected was analyzed for the impact of microsomal binding, using Langmuir and phase equilibrium binding models, and fitted to various inhibition models: competitive, noncompetitive, and mixed.
The competitive binding model identified binding of PPARγ to a degenerate DR-1 site as central to the inhibition of rabbit MMP-1 by rosiglitazone, and initial evidence suggested that the inhibition was due to competition between PPARγ and AP-1 for binding at the degenerate DR-1 site [ 17].
It can be shown that the total synergistic effect from all activators will disappear at high activator concentrations under the cooperative binding model (activator binding has already been saturated under this condition, thus cooperative interactions will not be further helpful), but not under the multiplicative model.
By clicking "Binding Model" and selecting specific models, users can select the other bindings and build up new bindings.
The exponential growth of the number of state variables with the number of binding sites and binding partners in conventional models is partly replaced by linear growth with the number of layers.
Prompted by this comment, we have re-evaluated fitting the Hill model to the binding data and used an alternative binding model (in the text and Figure 2d).
Data were fitted to a one-site binding model using Origin 7, and calculated binding parameters were ∆H = −15,890 ± 395 cal/mol, and ∆S = −29.9 cal/mol/deg.
