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We engineered site-specific AAG mutants to determine whether N169 prevents normal bases from mistakenly entering the active site.
The combined profile of wild type was compared with those of three long-lived mutants to determine how age-specific mortality is altered by mutations in age-1, clk-1, or spe-26.
We used deletion mutants to determine the specificity of the nCounter platform with our optimized hybridization conditions (3 µg total RNA).
We introduced an itsn-1 mutation into uev-1 mutants to determine whether it would suppress the accumulation of GLR-1 in accretions.
Some of these bacteria have well-developed and facile genetic systems for constructing mutants to determine gene function, and recombineering is a particularly effective tool.
Next, we utilized defined mutants to determine whether members of the M protein family are involved in adhesion to hexadecane (Table 1, Fig. 4&5).
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We used this new tracer protein mutant to determine the association behavior of aFGF with heparin in the presence of high concentrations of albumin that mimicked more closely the plasma medium in which aFGF is naturally located and in which it has evolved to function.
We over-expressed MPG1 in the ΔpdeH mutant to determine whether Mpg1 could restore the defects in surface hydrophobicity and pathogenicity.
We also analyzed the V162M mutant to determine whether there are consistent biochemical alterations among different disease-causing Rab7 mutants.
We crossed mtp5-2 thethe iar1-3 mutont to determine whether this allele also restored IAA-conjugate sensitivity to iar1.
We used how stru loss-of-function mutant to determine the implication of How in Rbf1-induced apoptosis.
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