Abstract
A model, based on receptor occupancy theory, for signaling due to receptor A and co-receptor B colocalization in the presence of a stable cell-cell interface reveals that a non-selective antagonist of receptor A with affinity for a receptor C on the trans-cell can induce as well as inhibit the signal due to A. As a result, assertion of selectivity for agents acting in such a system should be supported by measurement of signal when the co-receptor B is absent. For conditions where the co-receptor B is non-functional, the model reveals the potential to rescue function through bifunctional ligands, such as bispecific antibodies, antibody conjugates or even bifunctional tethered small molecules.
Supplementary materials
Title
Computed datapoints used to generate Figures 2, 4, 5, and 6
Description
The data generated by the KNIME protocol using the equations in the text that was used to generate the Figures in the text.
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