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Ojamäe et al. suggested a binding model in which the adsorbate binds to surface titan atoms through its carboxylic end (by the formation of an oxygen bridge) and to a surface oxygen ion through its ammonium end (by an H bond).
An alternative to a competitive model for binding of BrSA to the nonannular sites is a simple binding model in which lipid A (DOPC) does not bind significantly to the nonannular sites.
Recently, the existing lines of evidence have been incorporated into the selective binding model, in which selectivity of target gene activation and repression takes place directly at the level of DNA-binding, and the selective context model.
Finally, chemical cross-linking and protein docking studies support a competitive binding model, in which ToMOC and ToMOD compete for binding to the same region of ToMOH.
It was not possible to obtain a good fit of the data shown in Figure 2 to a simple binding model in which the site was either occupied by fatty acid or empty (eqs 12 and 14).
W88E(GM1) was titrated into a solution of CTB and the expected binding stoichiometry of one GM1os ligand per binding site was observed, which is consistent with a binding model in which W88E(GM1) forms a protein heterodimer complex with CTB.
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Other models of UPR activation are the ligand-binding model in which unfolded and/or misfolded proteins directly interact with the ER stress-sensing domains of the ER stress sensors, and the probing model, in which newly synthesized stress-sensing proteins probe the efficiency of the ER-resident protein-folding machinery by presenting themselves as substrates to the folding machinery [ 20].
We make use of a general binding model (21) in which E2C DBS1 denotes binding of an E2C homodimer to BS1 within DBS to form a binary complex, with an equilibrium constant KBS1, and E2C DBS2 denotes binding of an E2C dimer to BS2 within DBS to form a binary complex, with an equilibrium constant KBS2.
Notably, soaking of ClpX with nucleotides led to asymmetric binding, supporting a model in which ADP also binds asymmetrically to ClpB hexamers.
Overall, we observed that DNO supplementation improved BCO binding, consistent with a model in which efficient tag/anti-tag recognition is precluded by secondary structure in the BCO (Figure 4C), as well as with recent studies demonstrating oligonucleotide binding cooperativity between two oligonucleotides binding to adjacent sites on a single-stranded DNA [14].
The helix destabilizing mutants show that helix stability is important for membrane binding, further supporting a model in which F1 interacts with negatively charged membranes through formation of a transient helix in the loop region.
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