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The conservation of the β-Gal binding site may be a result of an evolutionary selection by HBGAs, as a prerequisite for viral survival.
It has been postulated that the σ2 receptor binding site may be located in the progesterone receptor membrane component 1 (PGRMC1), even if its MW (25 kDa) is different from that of σ2 receptor [10, 11].
In the extreme case, almost every predicted binding site may be considered "false positive".
Genetic variants that create or destroy an miRNA binding site may be the casual cis-acting eQTLs.
Our finding that hP2X4 (which formed a very low proportion of oligomers in detergent) bound to ATP-coupled beads implies that the presence of a partial binding site may be sufficient to permit ATP binding.
In contrast with the SAM/SAH binding site which is conserved among all SAM-dependent OMTs [ 14], the residues neighboring the other substrate binding site may be as variable as the compounds preferred by their OMTs [ 3].
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It is suggested that the spatial relationship between the multiple target binding sites may be important for restriction.
A large fraction of these flanking mutations change overall binding energies by an amount equal to or greater than consensus site mutations, suggesting that current definitions of TF binding sites may be too restrictive.
These differences in binding sites may be related to the opposite polarity of translocation on MTs of the motors.
The data suggests that the hepatocyte binding sites may be overwhelmed by this dose and/or injection rate of MnDPDP.
For intermediate PTX concentrations (≥10 nM), saturation of microtubule binding sites may be further increased, leading to G2/M arrest and apoptosis [38].
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