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Using (R -selective amine tR -selectivefrom aminegillus transaminaseATA) as a transaminase model, in silico design was applied employing B-fromor Aspergillus free energy (ΔΔGfold) calculaterreus
Using this native model, in silico mutations were introduced corresponding to those described in this study.
Analysis of this model in silico resulted in predictions that we could test experimentally.
Using this metabolic model, in silico metabolic flux analyses were performed to investigate the effects of various environmental and genetic variables.
For the analysis of the genome-scale metabolic model, in silico flux analysis was used where the internal metabolites were first balanced under the assumption of pseudo-steady state [ 34].
The objective of the model (in silico cell) was growth and the constraints were set to represent the environmental conditions and the flux through the ammonium exchange reaction was calculated using linear optimization at steady state.
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Replacement means conducting experiments using nonanimal models, such as in vitro method with cell culture as well as with computer model simulation (in silico), whenever possible.
The enzyme mode of action, modeled in silico, demonstrates a processive multiple attack mechanism.
Current studies using the ascidian embryo benefit from extensively annotated genomic resources to characterize transcript models in silico.
An optimised scaffold geometry was modelled in silico via a laser scanning data set from a patient who underwent breast reconstruction surgery.
Modeling in silico indicates that the phosphorylated forms of PT3 and PT5 fit well into the PLP-binding site of plasmodial ornithine decarboxylase (PfODC), the key enzyme of polyamine synthesis, consistent with the ability to abolish ODC activity in vitro.
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