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TFB1M (transcription factor B1), encoding a mitochondrial rRNA methyltransferase, has been putatively identified as a possible nuclear modifier of the m.1555A>G mutation, suggesting a connection between 12S rRNA methylation and hearing loss (Raimundo et al., 2012).
None of the single mutations was able to abolish Nrf2 phosphorylation as well as the combined 5A mutation, suggesting a redundancy in phosphorylation sites (Figure S1).
The sample from August 7 did not contain this mutation, suggesting a de novo H275Y substitution secondary to oseltamivir use.
The effect on catalase activity was independent of disease progression, represented by mouse age and α-Syn mutation, suggesting a potential physiological function for α-Syn.
The twofold increase in resistance conferred by a gsiB deletion is less than that of the gsiB point mutation, suggesting a more complex situation.
PDB patient carriers of a post-zygotic mutation had a lower number of affected bones and Renier's index than patients carrying a germinal mutation, suggesting a lower disease extension.
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The extreme example of this is the T72c2 cell line where, of the 30 plaques sequenced, 28 carried the same mutation, suggesting an event that occurred very early after transfection and selection.
Surprisingly, suppression of apoptosis upon oxidative stress treatment as seen upon SNEV overexpression was completely abolished by S149A mutation, suggesting an important role of ATM dependent phosphorylation of SNEV for induction of apoptosis.
In contrast, when six oncogenic mutations are required for cancer (C = 6), α50% ranges from 11 30 (Supplementary Table S1), in the lower range of commonly observed values of mutation rate increase due to mutator mutations, suggesting a predominance of mutator pathways, in that most mutator mutations would then correspond to α>α50%.
In contrast, when six oncogenic mutations are required for cancer (C = 6), α50% ranges from 11 30 (Supplementary Table S1), in the lower range of commonly observed values of mutation rate increase due to mutator mutations, suggesting a predominance of mutator pathways.
A long remission following TKI treatment and conservation of the original activating EGFR mutation suggests a transformation rather than a coexistence of SCLC and NSCLC.
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