(Supplementary file 2 lists all the mutations for each mutated episome).
> -wrap-foot> Furthermore, as Figure 3 shows, the distribution and frequencies of the Leu-binding mutations for each of the seven GrsA-PheA mutatable residue positions is significantly different for traditional DEE, B RDEE and BD.
Specific mutations for each cancer as well as the percentage of mutated BRCA1 DNA (m%), NM_score, and ER status for each cancer is shown in Additional file 5.
Here, we described 19 novel variants, bringing the total to 53 causative mutations (Fig. 2A). Figure 2B shows the relative richness of (i) distinct mutations for each exon (solid line), as well as the frequency of (ii) mutated alleles for each exon (dotted line).
Potential driver mutations were analyzed to determine common driver mutations for each patient (Supplementary Table 4).
VarScan2 somatic algorithm version 2.3.2 (ref. 51) was used to call high-confidence somatic mutations for each patient.
Table 2 lists the top ten mutations for each dataset.
We identified additional somatic coding region mutations for each of the genes in the melanoma samples.
The number of mutations for each subtype is expressed as a proportion of the total number analyzed sequences for that particular subtype (Table 2).
Single mutations for each individual residue in the αK helical region and double/quadruple mutations for hydrophobic residues did not change the Golgi/lysosomal localisation of EGFP-Irgm1 αK.
We assumed mutations for each fitness component were independent.
