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If there was an inhibitory effect of up-regulated PrP on IMERV, then PrP-deficient mice should show sustained IMERV activity.
If Tregs suppress NKT cells, the Treg-depleted mice, compared to undepleted NKT KO mice, should show no enhancement in the CD8+ T cell immune response.
In the system presented in this study, TET-GFP mice should show a reduction in GFP+ cells in response to continuous doxycycline (dox) treatment as the dox causes the tTA to be released from the TRE and H2B-GFP expression is lost.
If p21 was involved in neuroprotection after hypoxic exposure, preconditioned p21-/ mice should show an increased susceptibility to light damage as compared to wild type mice.
If oxidative stress was a major mechanism of age-related mitochondrial dysfunction then mitochondria from aged Sod2+/− mice should show increased mitochondrial dysfunction compared to aged WT mice.
Therefore, if AChE-S suppression could by itself prevent stress-inducible cognitive decline, TgR mice should show no such decline; but if miR-132 increases are the cause, then these mice should present a stress phenotype.
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For SNPs, where HAB and LAB mice would show the opposite genotype homozygously, F1 mice should exclusively show heterozygous genotypes.
These mice should not show any H2B-GFP expression prior to being crossed to the TET-off mice because no tTA protein is present to drive GFP expression from the TRE.
The knockout mice, by their deficiencies, should show what the lost gene does.
Since we showed that the TFBS sites are generally NOT co-located exactly with the mature miRNA sequence (Table 7, now Figure 4), there is no reason to assume that the set of conserved pre-miRs [defined by overall similarity across rat, mouse and human] should show the detailed conservation of exact TFBS motifs that it does, nor that it should extend to other vertebrate classes.
We hypothesized that if the severity of addiction were related to the intensity of these markers, then WT-HR mice should have shown more compulsive changes over time than WT-LR mice.
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