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However, our findings also suggest an essential function for HEX in the early stage of hepatic specification, which differs from the results obtained with mouse embryos showing that HEX is not necessary for liver bud induction [ 33].
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The first chimeric animals were created by researchers in the 1960s, when experiments with mouse embryos showed they could combine to form a single mouse of normal size.
Since PC5/6-knockout mouse embryos show developmental abnormalities, and reduced overall mineralization, we designed this study to determine whether OPN is a substrate of PC5/6.
Examination of mouse embryos showed that Cre-mediated recombination in the developing brain caused an increase in cell death.
Moreover, Hes1−/− mouse embryos showed a significantly smaller total thyroid surface area (−40 to −60%) compared to wild type mice at all study time points (E9.5−E16.5).
Transcriptional profiling of topo IIβ knockout mouse embryos showed that the enzyme regulates only a small fraction of genes (1 4%) in the late embryonic brain cells [7].
Both Tgfb2−/− and Pax6+/− mouse embryos show similar defects in their eyes; specifically, the lens does not separate from the cornea [21], [23], [45].
Interestingly, a detailed analysis of γ-wt expression in mouse embryos showed that while the protein was virtually absent from trachea and large bronchia, it accumulated in the bronchioli (Figure 1Dii).
A comparative analysis of Twist mRNA and Twist protein expression in mouse embryos showed abundant Twist RNA expression in presomitic mesoderm, epithelial somites, and anterior mesoderm, but no Twist protein could be found in those tissues [9].
Adar1 mutant mouse embryos show aberrant interferon induction and die by embryonic day E12.5.
Isl1 null mouse embryos show developmental anomalies at E9.5 and die at E10 [ 24].
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