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In Seppälä et al. (2010), the dominant topologies of EmrE mutants are determined by measuring the growth of E. coli cells in the presence of ethidium bromide (EtBr).
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Some of the mutants were determined as superiors for the studied variables.
Binding changes of the individual mutants were determined using three saliva samples that are Lea (Nonsec/Lea), Ley (Sec/Ley) and Leb (Sec/Leb) positive, respectively (Fig. 8B).
The metal contents of the wild-type enzyme and mutants were determined by inductively coupled plasma optical emission spectrometer (ICP-OES), PerkinElmer 5300DV.
The structures of PKM2 mutants were determined by molecular replacement using the monomer of PKM2 wild-type structure (3BJT.pdb) as a searching model (Christofk et al., 2008b).
The nucleotide sequences of entire acrR, marR, and soxR genes in organic solvent-tolerant mutants were determined by DNA sequencing to identify mutations in these genes.
However, in order to confirm that the low gluconic acid production was not caused by different growth rates of the Δgox mutants, the biomass of the Δgox mutants was determined after the growth experiment.
T m (melting temperature) values of CueO and its mutants were determined by differential scanning calorimetry (General Electric Company, Louisville, KY, USA) using ≥ 400 μg of sample per milliliter (Jian Tian et al. 2015).
The structures of the complexes in several pil mutants were determined.
The feeding ability of itpr mutants was determined quantitatively by measuring ingestion of colored food (Figure 2).
Deleted regions in the genome of these mutants were determined by sequencing of the PCR fragments from their genomes.
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