First, non-synonymous changes in non-contact residues may alter the contact region with the T-cell receptor, with consequences for antigen specificity [ 12].
Similarly, naturally occurring defects such as osteochondrosis lesions may alter normal contact mechanics in affected joints.
Small changes in antibiotic structure may alter the contacts with the enzyme and consequently change the point for inhibition, as illustrated by the case of rifamycins [ 10].
Polymorphic variants may alter their nearby bonding contacts by changes of volume or polarity, as in absence/presence of a salt bridge to Arg 506 with the extension of 503′s side chain between alleles SDI and SEI.
Exposure to the environment (UV, water and air contact …) may alter the physicochemical properties of surface-modified CeO2 NPs, such as the chemical structure of the surface, size, shape, and dispersion state, which are important parameters for toxicity.
Other behavior may change during a pandemic; e.g., people may alter the number and duration of contacts, with degree of alteration changing as the pandemic progresses.
Studies in humans and other primates suggest that direct contact during social interactions may alter the composition of the gut microbiome in an individual.
In fact, tumor cells may alter the surrounding stroma through direct cell contact or via the secretion of paracrine soluble factors, inducing cell differentiation or extracellular matrix modifications [ 9].
Indeed, disruption of vimentin filaments has been shown to result in loss of cell contact with the surrounding matrix which may alter the signaling dynamics of the cell and in effect shut down transcriptional events [ 24].
This observation may be related to the fact that F764 makes direct ligand contact [37], and its replacement by ligand may alter the conformation of the ligand binding pocket which results in increased affinity for ligands other than DHT.
