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These copy number changes show a positive correlation with average transcript levels of resident genes.
All individual transcript levels, the global average transcript levels, and pmi were log10 transformed prior to inclusion in analyses.
The additional copy of this chromosome directly and significantly increased the average transcript levels of genes residing on Chromosome 7 [12].
As in primary tumors, an increase in genomic copy number resulted in increased average transcript levels of genes residing on the aneuploid chromosomes.
The pom1 expression levels are ∼3.8-fold below average transcript levels [19], and repressed Purg1-pom1 levels were ∼90% of the native pom1 levels (based on microarray data).
This result demonstrates that the average transcript levels of genes within a given CRE expression category correlate with the strength of that category.
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The 5'-UTRs alone had no influence on the average transcript level compared to the control variant (No. 2 and No. 5 in Figure 2A).
For this reason, we examined the time that was needed to reach the level of 4-fold increase in the average transcript level of the Atf1/Pcr1-bound induced and Atf1/Pcr1-unbound induced genes.
Using the microarray data obtained from these seven samples, we calculated the average transcript level for each gene at each time point (i.e., immediately after mixing bacteria with donor human blood, and after 30 and 90 min of incubation) for the 1,995 ORFs present on the chip [13].
The average transcript level of all genes in each cluster at each time point in the light relative to the average transcript level in the dark are given in Figure 3B.
However, this was contrary to the notion that the transcript level of the ideal reference gene must be close to the average transcript level of the GOIs.
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