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Therefore, the peptides binding models have been developed for a very limited number of HLAs.
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In similar cases of predictor development such as for GPI lipid anchoring [ 17], N-terminal N-myristoylation [ 20], prenylation [ 21] and peroxisomal targeting [ 22, 24], our simplified substrate protein binding model has been successfully applied.
Moreover, a semiempirical tight-binding model has been appropriately calibrated for transport calculations on these clusters.
We also summarize the descriptors based on which the HLA peptide binding prediction models have been constructed and discuss the limitation and challenges of the current methods.
As both P3 and DY are essential for repression through binding of PTB, models have been suggested in which there are looping interactions between proteins bound to the two regions.
Although such models provided relatively accurate predictions for short binding motifs [ 14], alternative models have been developed to encode short-range information through building much larger matrices for subsequences (k-mers) [ 5, 15].
Various statistical and computational models have been developed to characterize binding affinity [ 10, 11].
These models have been shown to display DNA binding abilities strongly dependent on stereochemistry.
Several models have been published for describing the binding of solute molecules to functionalized surfaces.
Regression models have been developed for quantitative predictions of HLA peptide binding.
These models have been developed further to account for the physical binding properties of the probes.
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