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The relative abundance of the various VEGF splice variants was determined by RT-PCR using cDNA available in our laboratory.
Native molecular mass of MtbMfd and its variants was determined by gel filtration chromatography.
Using subcellular fractionation, the cellular localization of wild-type and PepD variants was determined.
The relative number of gene variants was determined by dividing the number of genes belonging to each functional category by the total number of genes detected [34].
The affinity of the G12 moAb for different hexapeptide variants was determined in a competitive assay in which immobilized gliadin was challenged with QPQLPY-derivative peptides as soluble competitors (Figure 4A).
Residual inhibition by SFTI-FCQR variants was determined in competitive kinetic assays (as above), adding a volume of media to give 10 nM SFTI-FCQR Asn14 or 25 nM SFTI-FCQR Lys14 at 0 hr.
Similar(29)
TPH allelic variants were determined in each subject using a PCR-based technique.
Gβ3 allelic variants were determined in each subject using a PCR-based technique.
SERPR allelic variants were determined in each subject using a PCR-based technique.
Stability changes for the toxin variants were determined using circular dichroism and fluorescence measurements, and scanning calorimetry.
The kinetic rate constants and equilibrium dissociation constants for monomeric and dimeric ecotin variants were determined with both trypsin and chymotrypsin.
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