Among the founder clone mutations, we noticed a BRCA1 nonsense mutation, which may explain the high mutation rate observed in this sample.
While examining the above point mutations, we noticed that channels with substitutions at Gly showed unusual characteristics on extended pressure applications.
Furthermore, by carefully examining luminal breast cancer cases with RUNX1 mutations, we noticed that >50% of them are accompanied by mutations or deletions in either TP53 or RB1 genes (Cancer Genome Atlas Network, 2012).
In previous studies of the Tau-ΔK280 mutation we had noticed pronounced aggregation, but it was not clear in what pathway the major effect of mutant Tau was located.
Although we observed only a weak correlation of somatic mutations and gene expression for RTKs, we noticed a remarkable correlation for mutations in adhesion molecules with gene expression (Table 3).
Interestingly, we noticed TP53 mutations with high allelic fraction in low cellularity tumors.
We noticed that mutations at several sites resulted in amino acid changes, which were maintained in influenza proteins for a relatively long time.
We noticed that mutations in the conserved residues in the NBD of the Ssa proteins affect the tRNA binding ability in vitro differently between Ssa1p and Ssa2p.
Accordingly, we noticed that mutations in components of the Doa10 complex have a mild growth phenotype when grown at low temperatures (10°C), as previously reported (Loertscher et al., 2006 and data not shown).
We noticed that a mutation can affect changes only on 1 3 strands in a probe; thus, best efforts were made to minimize the number of such operation calls by storing the results and making them inheritable by mutated individuals.
