Thus, inhibition of these feedback and feedforward loops, and inhibition of different nodes of the PI3K pathway, does not affect the degree of PTEN association with p85α or WWP2, suggesting that the PTEN interactions with p85α or WWP2 are unlikely to be explained by mutant-triggered changes in PI3K downstream signaling or regulatory loops.
The selection coefficient obtained by competing mutants expressing YFP against a GFP reference strain can be explained by the mutant genetic background or by YFP expression itself.
However, we do not know whether the difference to paraquat can be explained by different mutant SOD1 (G85R and A4V vs. G41S), or experimental conditions (20 mM paraquat in cornmeal fly food vs. 40 mM paraquat in 1% sucrose).
In summary, development of a primary intracerebral mesenchymal neoplasm in a child with NCMS and hemimegalencephaly can likely be explained by specific NRAS mutant mosaicism possibly in combination with a MET germline variation, which together constitute a unique combination.
Three of them could be explained by a low mutant allele content (<20%) which is below the Sanger sequencing sensitivity and therefore the mutation could not be detected using this technique.
Therefore, the slowing of the catalytic cycle could be explained by either the mutant gem-diamine complexes being in a more stable form (in an energy well) compared to the wild type enzyme or by an increased energy barrier to pass to the external aldimine.
The variance observed cannot be explained by selection of mutants from within the bacterial population, as 'selected' bacterial clones isolated from terminally infected subjects did not show enhanced virulence in subsequent infection experiments.
When we examined the number of genes and the GO terms they represent in the double mutants compared to the single mutants, we conclude that Gcn5, Mst2 and Elp3 are functionally redundant in repressing transcription because the number of terms enriched in the double mutants cannot be explained by adding the single mutants' terms together.
These cases cannot be explained by the selection of mutant tumor cells, and the precise mechanisms underlying this clinical drug resistance are ill-defined.
The difference in time to death between the two HD171-eGFP lines of mice and the HD-N171-82Q line 81 mice can be explained by the level of mutant htt expression.
Although some of the wild-type sequences detected in this experiment may also be explained by the ADO of mutant alleles, it is obvious that the large number of wild-type sequences detected in melanoma tissues cannot be explained by ADO alone.
