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We found that intergenic and genic sequences have opposite relationships with respect to both expression variability and expression level, and that this does not hold for coding sequences when considered individually.
In summary, GC3 is positively correlated with both expression variability and variation in genic methylation.
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Although polymorphisms within several genes have previously been associated with both gene expression variability and MetS components [ 5], epigenetic mechanisms may also contribute to this variability.
Our results highlight the influence of gene network architecture on expression variability and implicate feedback regulation as an effective mechanism to ensure developmental robustness.
Moreover, we found similar results for expression variability and for noise.
Figure 5.B points to a strong correlation existing between the level of expression variability and the extent of disease association.
In summary, as suggested by our results on differences of expression variability between the two clinical types, expression variability can classify the two subtypes remarkably well, pointing to a potentially important relation between expression variability and disease aggressiveness.
Partial correlations between gene expression variability and methylation and between GC3 and gene expression variability are much smaller than the full correlation coefficients.
There are strong relations between gene expression variability and disease subtype linking significantly increased expression variability to phenotypes such as aggressiveness and resistance to therapy in CLL.
We compared the fragility of transcriptional regulatory program with other determinants of expression variability, and showed that the fragility is an important source of expression variability.
This is consistent with our observation of a positive relationship between gene expression variability and GC3.
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