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This review also examines progress toward the goal of achieving a comprehensive understanding of the chemical and physical basis for molecular recognition of viral surface proteins in order to build predictive molecular models that can be used for vaccine design.
Here, we describe a bottom-up approach to design two computationally mutated molecular models that use non-covalent interactions to cross-link triple helices of tropocollagen molecules and thus promote self-association.
In this work, transport properties of monomethylamine, dimethylamine, dimethylether and hydrogen chloride are predicted by molecular simulation, employing rigid, non-polarizable molecular models that were developed without using any transport property information.
These differences have been interpreted on the basis of DFT (B3LYP/6-311++G**) conputationsuitabletable molecular models that allowed a qualitative and quantitative rationalization of the chemical physical effects involved.
Based on the crystallographic analysis of TIFF3 there are 3 different molecular models that slightly vary in their inter-domain configuration.
To illustrate this point, we present two molecular models that are each consistent with our findings, but which suggest two completely different interpretations for the significance of an interaction between ICP0 and ICP4 in the biology of HSV infections.
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We propose here a molecular model that accounts for periodic calcium spiking induced by a constant stimulus.
Here, we propose a molecular model that reflects the essential features of the Drosophila circadian clock to clarify the different roles of negative and positive feedback loops.
The experiments and the molecular modelling that supports them, and which provides mechanistic insights, have been carefully performed.
This report is the first to present a multi-purposed, molecule-based molecular model that can characterize as many as 24 different human tissue types.
It has been suggested, based on molecular modelling, that when Bim binds to Bax, it displaces helix 8 owing to a clash between C-terminal regions of the BimBH3 and T167 on Bax.
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