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The single-molecule conductance of carboxylic acid binding to bulk metal electrode was also studied, and has almost the same value as that binding to Pd nanoclusters.
In addition, we show that binding to poly-Ub and, to a lesser extent, to monoubiquitin increases the stability of the NOA coiled-coil dimer.
We show that binding to F-actin induces a conformational change in plectin that is inhibited by an engineered interdomain disulfide bridge.
Data are reported in Fig. 6, and show that binding to wild type CHO-K1 cells was greatly enhanced for CXCL12γ compared to CXCL12α.
Tracer binding was investigated to verify that binding to the inflamed synovium was mediated through TSPO.
Thus, one possibility is that binding to LDL-apoB100 stabilizes a native autoinhibited conformation of PCSK9.
The implication is that binding to ICAM-1 is associated with CM.
This presumably reflects that binding to HSPG was competed by heparin.
Do biased ligands (ligands that binding to the same receptor but activate different signalling pathways) exist for ET receptors?
We could show that binding to unmodified H3R2 via the PHD and ubiquitination of H3K18 via the RING domain are required for UHRF1 to mediate maintenance DNA methylation.
It is suggested that binding to membrane phospholipids controls α-Syn structure, physiology and pathogenesis.
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