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The data for each ITC titration are well-fitted to a sequential two-site binding model rather than a simple one-site or two-site mode (Fig. 7A-C and Supplemental Table S2).
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It will act as role model rather than leader.
Nevertheless, this genotype phenotype correlation is based on the analysis of structural models rather than on the investigation of the DNA-binding properties of IRF6.
While this genotype phenotype correlation has broadly been supported by subsequent studies, it is based solely on the analysis of structural models rather than on a systematic investigation of the DNA-binding properties of IRF6.
Study findings based on modelling rather than actual patient data.
Health outcomes were modeled rather than directly assessed.
However, by using predicted TF binding sites rather than observed sites, these models achieved limited accuracy at predicting human cell type-specific expression changes.
Here, we show that the decoding bases flip on a timescale faster than that of gentamicin binding, supporting a stochastic gating mechanism for antibiotic binding, rather than an induced-fit model where the bases only flip in the presence of a ligand.
7 and 8) consistently yielded a better fit of the autocorrelation functions than the diffusion model (χ ∼30% smaller, Table 3), supporting the notion that the dynamics in adhesive regions is dominated by binding equilibria rather than diffusion.
Taken together, these findings suggest that GAG binding rather than CXCR3 binding is important for CXCL10's anti-proliferative effect.
We hypothesize that they target the nucleotide (ATP) binding site rather than the expected cytoplasm-accessible pocket.
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