Comparison of ubiquitination levels of overexpressed GFP-H3 carrying R2A, K18A or K23A mutations suggests that in this constellation K23 could also be modified (Supplementary information, Figure S5B).
The three DsbG variant strains that expressed the highest level of PhoA* contained three to six mutations suggesting that in these cases more than one mutation may contribute to their strong phenotype.
Although double or triple mutations suggested poor prognosis in training group, they were not proved in validation group (Supplementary Fig. 2).
The predominance of transition mutations suggests that TP53 mutations in ovarian carcinomas arise because of spontaneous errors in DNA synthesis and repair, rather than the direct interaction of carcinogens with DNA.
The close proximity of these two mutations suggests that a mutation in this region of GDH1 may yield a phenotypic trait that has been selected for through GS evolution.
In addition, the lower penetrance of these mutations suggests that they might act in concert with other hereditary factors [ 6- 10].
However, our result show that antioxidants do not improve cardiac abnormalities caused by dOpa1 mutations, suggesting that these mutations result in cardiac dysfunction primarily by affecting mitochondrial ATP production rather than by increasing ROS production.
The mutual exclusive occurrence of KRAS and BRAF mutations suggests they occur in different tumor subtypes [ 12].
The apparent K d L-ser is unchanged by the incorporation of the HSAN1 mutation, suggesting that, in this case, the key L-serine external aldimine intermediate is formed in the same way as in the native SPT.
Furthermore, both host mutants show efficient suppression of the cIII mutation, suggesting that in the absence of FtsH and HflKC, CIII is dispensable.
However, we find that knockdowns of splicing factors instead enhance weak fog-1 mutation, suggesting that in addition to regulating FOG-1 production, splicing machinery is important for FOG-1 function.
