We show by coprecipitation that five cancer-derived IDH1 R132 mutants bind IDH1-WT but that three cancer-derived IDH2 R172 mutants exert minimal binding to IDH2-WT.
Conversely, only minimal binding of Sal5 (<3%) to dead cisplatin-treated cells was observed (Figure 2B).
The minimal binding sequence of p6.7 was confirmed experimentally by synthesis of progressively deleted peptides.
Systematic mutagenesis further demonstrated that tyrosine surfaces across four or more β-strands formed the minimal binding site for ThT.
In contrast, the control EMT6 cells, which do not express the CA125 antigen, showed minimal binding of the bfFp.
Specific binding of terminal phosphate groups with minimal binding of the internal phosphate diesters has been demonstrated.
Maximum binding was found in the thalamus, while moderate binding is seen in the cortex, and minimal binding in the cerebellum.
An alanine scan of the 13-residue epitope 3D7-MSP2207 222 identified the minimal binding epitope of 4D11 and the key residues involved in binding.
In vitro fluorescence microscopy evaluation of cKNGRE-OG demonstrated binding and active uptake by CD13+ cancer cells and minimal binding to CD13− cancer cells.
With the aid of the minimal binding scheme, the ACO actions on IK DR) was quantitatively provided with a dissociation constant of 0.6 μM.
ZNF198 exhibited minimal binding to HDAC1 alone.
