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Prior to making transgenic mice, we tested whether ES clones overexpressing Hdac6 show resistance to adenovirus infection.
To follow bacterial dissemination during plague infections in mice we tested the possibility of using bioluminescence imaging (BLI), an alternative non-invasive approach.
As 6-OHDA is widely used to induce parkinsonal phenotypes in mice, we tested the functional implication of parkin for PD after 6-OHDA treatments.
Using Pompe (Gaa mice, we tested the hypothesis that intralingual delivery of viral vectors encoding GAA results in GAA expression and glycogen clearance in both tongue myofibers and hypoglossal (XII) motoneurons.
Additionally, the mice we tested showed alterations in the ERGs (Figure 4) that were consistent with previous findings [22], [30].
Using mice, we tested the hypothesis that dietary experience during childhood and adolescence affects adult obesity risk.
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IDC13 and IDC78 but not IDC16 increased life expectancy of mouse we tested, whereas SR protein depletion is detrimental for survival [24].
Sle2c2 mice, which we tested by comparing their response to exogenous G-CSF.
In vitro screening for mouse tumor cell lines revealed that all mouse lines we tested exhibited comparably low susceptibility to infection by our attenuated mutant virus, on par with normal quiescent human cells.
Here, employing the telomerase-deficient mouse model, we tested whether the NHEJ component DNA-dependent protein kinase catalytic subunit (DNA-PKcs) was required for fusion of eroded/dysfunctional telomere ends and the telomere checkpoint responses.
After demonstrating gene expression for notch-1, notch-2, notch-3, and the Notch ligands jagged-1 and jagged-2 in embryonic mouse lung, we tested whether altering expression of these genes can modulate branching morphogenesis.
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