To compare the effect of APP K16N with other FAD mutations we utilized the arctic mutation E22G which is located close to the α-secretase cleavage site.
To screen lethal piggyBac and P insertional mutations, we utilized two collections from the Drosophila Genetic Resource Center DGRCC, Kyoto, Japan), where insertion mutations had been recombined on FRT chromosomes (Chen et al. 2005; Schuldiner et al. 2008).
In order to identify underlying mutation rapidly, we utilized next-generation sequencing in a four-generation Chinese family with RP.
To study the impact of inoculums on detection and mutation frequency, we utilized a high inoculum of S. aureus (1010 CFU/ml) which is often observed in the severe S. aureus infection including infective endocarditis.
To gain insight into how specific Met mutations induce tumorigenesis, we utilized the panel of knock-in mutations we previously generated.
To determine the extent to which exposure to Mn2+ increases the accumulations of mutations and to quantify the increase in the mutation rate of wild-type yeast cells, we utilized the CAN1 forward mutation assay [ 33], as described in Section 2. As shown in Figure 4, the mutation rate increased 12-fold (from 1.9 × 10−7 to 23.1 × 10−7) when wild-type cells were treated with 1.5 mM Mn2+.
To compare the consequences of oncogenic mutations in different tissues, we utilized a well-characterized system to induce tissue-specific tumors in Drosophila melanogaster using oncogenic Ras (Brumby and Richardson, 2003; Dow et al., 2008; Humbert et al., 2008; Pagliarini et al., 2003).
First, we utilized the mutation positions from COSMIC data to map the gene regions using the UCSC Genome Browser based on the GRCh37 genome annotation [ 28].
Although our data demonstrate that the AIE domain is critical in regulating the phosphorylation states of eNOS, we utilized deletion mutations in our studies which can potentially generate a wide range of effects.
