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In addition, the analysis of the interaction between SOD and small drug molecules is interesting to some extent, because the binding of specific small molecules to SOD has only been characterized in detail for a few examples [23, 24].
However, the enzyme levels are often increased by exposure of the animals to xenobiotics, because the binding of antioxidant response element (ARE) and Nrf1 and Nrf2 proteins allows increased transcription of gene encoding GSTs [35].
This is because the binding of drugs to plasma proteins (like human serum albumin, lipoprotein, glycoprotein, α, β, and γ globulins) greatly reduces the quantity of the drug in general blood circulation and hence the less bound a drug is, the more efficiently it can cross cell membranes or diffuse.
However, transcription initiation does not proceed from promoters having strict consensus sequences, because the binding of the RNAP to a perfect consensus promoter is so strong that it prevents the necessary steps towards promoter clearance and elongation initiation [11].
Most importantly, we found that the interaction between bcl-2 and HIF-1α proteins was not dependent on HSP90 inhibition, because the binding of bcl-2 and HIF-1α was not reversed by the treatment with 17-AAG.
Because the binding of sugars to hSGLT3 causes membrane depolarization and not sugar transport, it has been suggested that hSGLT3 functions as a sugar sensor instead of a sugar transporter [3].
Similar(29)
The following introduction of streptavidin resulted in fluorescence quenching (fluorescence decrease) because of the binding of hybridized DNA biotin with streptavidin.
This was attributed to a higher thermoresistance of the albumin component, most probably because of the binding of uremic toxin to HSA.
Because of the binding of HIV-1 to contaminating leukocytes (Fig. 3A), the question arose whether the apparent binding of HIV-1 to non-hemolyzed cells actually consisted of binding to the small number of contaminating CD4 cells.
Under this condition, there is insignificant remodeling of the HDL particles because of the binding of apoA-I.
This indicates that FRET occurs because of the binding of the target molecule to the DNA probes.
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