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Here we investigate the molecular basis of this phenotype by comparing the cellular level of three RNA polymerase sigma subunits by immunoblot analysis.
Characterization of the molecular basis of this phenotype in three previously uninvestigated families has shown that the most common genetic basis of GPC/D deficiency is deletion of exons 3 and 4 of the GPC gene.
As these observations point to a functional importance of BicD phosphorylation, we set out to study the molecular basis of this phenotype.
To corroborate this inference, we examined the cellular basis of this phenotype in greater detail.
The mechanistic and genetic basis of this phenotype in primary human B cells remains uncertain.
Together, these results strongly support the model that the molecular basis of this phenotype arises in early development.
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The molecular basis of this extremophile phenotype, involving strain isolates with a 3-4 ofder of magnitude increase in IR resistance at 3000 Gy, is now addressed.
To investigate the genomic basis of this exceptional phenotype, we obtained a de-novo genome sequence of the species type-strain and analysed its transcriptomic response to conditions close to the limits of its lower and upper salinity range.
They could then use this information to enhance their understanding of the molecular basis of the phenotype(s) they had observed.
However, on the basis of the phenotype in Esrrg−/− mice, it is very unlikely that this gene product has a non-redundant role in nephron development.
Chaiworapongsa, T. et al. Differences and similarities in the transcriptional profile of peripheral whole blood in early and late-onset preeclampsia: insights into the molecular basis of the phenotype of preeclampsiaa.
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