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Unexpectedly, a substantial fraction of strain-specific factor binding could not be explained by local mutations.
Genetic information about the TSPO binding could not be obtained because knowledge about the importance of genetic background for TSPO binding was not available at the time the study was performed.
In wildtype cells, IIH6C4 immunoreactivity and laminin binding could not be detected from total lysate (Figure 2B).
Although the binding affinity of G27, G125, and G9 ranked the lowest among all the anti-CAIX antibodies selected (Tables 2 and 3), their binding could not be blocked completely by any other antibodies.
Unspecific tetramer binding could not be blocked by CD8α antibody.
Hence, the possible contribution of these residues to antagonist binding could not be validated experimentally.
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This may be compared to a 60-fold increase demonstrated for 1. Attempts to fit these small spectral changes to binding models failed to produce reliable saturation binding curves and thus a DNA binding constant could not be derived for 2 using this latter technique.
It was found that the binding isotherm could not be fitted to the simplest binding model, but fitted into a sequential binding model suggesting that the interaction involves non-symmetric binding to the two AnxA2 peptides: one binding site on the dimer needs to be occupied before the second binding event can take place.
Intriguingly, the bioinformatics analysis also revealed the presence of miR-24-2 binding sites in BCL-2 and MDM2 mRNA besides having two binding sites in H2AFX mRNA, however, the binding site could not be identified in P21 mRNA.
Unfortunately, due to protein instability of NleH1ΔC4, the role of the PDZ binding motif of recombinant NleH1 in binding NHERF2 could not be investigated.
For SLII, the difference in binding affinity with or without U2A′ is small, such that U2A′ binding affinity could not be extracted from these experiments.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com