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Third, the mutation is designed to occur.
In site-directed mutagenesis, an oligonucleotide encoding the desired mutation is designed with flanking sequences either side that are complementary to the target sequence and these direct its binding to the desired sequence on a template.
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In the grouping genetic algorithm, the initialization, crossover and mutation are designed according to our problem's characteristics.
In the AGCUK algorithm, noising selection and division absorption mutation are designed to keep a balance between selection pressure and population diversity.
This mutation was designed to disrupt the CR2 C3d interaction, either directly through steric inhibition, or indirectly through disruption of a physiological dimer.
For this specific problem, the fitness function, the algorithm of genetic selection, crossover and mutation are designed to ensure the diversity of kernel function and more selected chances of optimal individual in evolution process.
For simplifying the process of cell disruption and immobilization, the lysis genes of phage λ (S−RRz) with the S amber mutation were designed to introduce into the over-expression system of GLA.
The PRH F32E mutation was designed to inhibit the binding of PRH to TLE1.
Primers for the mutation were designed as mismatch primers to the nucleotide site of interest.
Two complementary oligonucleotide primers containing the desired mutation were designed for each point mutation (Supplementary file 5).
This switch mutation was designed to restore the bulk and hydrogen bonds observed between WT-FIH and WT-CTAD.
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