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Mutant animals displayed posterior transformations along with subtle deregulations of Hoxd genes, indicating an impact of the centromeric landscape on the fine-tuning of Hoxd gene expression.
Furthermore, αSNAP-deficient mutant animals displayed reduced formation of lysozyme granules in small intestinal crypts and decreased expression of lysozyme and defensins in the intestinal mucosa, which is indicative of defects in Paneth cell differentiation.
Trpml3 Δ/Δ mice inherited the mutation stably and homozygous mutant animals displayed normal breeding performance.
AMPK mutant animals displayed starvation-like lipid accumulation patterns in metabolically key liver-like cells, oenocytes, even under fed conditions, consistent with a persistent starved state.
Conversely, daf-18 mutant animals displayed a significantly increased glycogen consumption rate relative to wild type.
Compared with controls and Bcl11b mutants, Dsp mutant animals displayed no overt changes in mossy fibre distribution (Supplementary Figure S7A and B).
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Ngn2 null mutant animals display a reduced size of the cornu ammonis and a malformed DG (Figure 3 and 4; [20]).
Clock/Clock mutant animals display several interesting phenotypes in addition to overt loss of circadian rhythms in locomotor activity [8], [27].
The Lmod3 PB/PB mutant animals display severe muscle weakness in addition to growth retardation.
A previous attempt to generate such a model through gene-targeted ablation of Col3a1 was of limited success, despite homozygous mutant animals displaying both bruising and aortic dissection.
As already reported in previous publications [ 19, 20] at 20°C the fat-6;fat-7 double mutant animals display a greatly reduced fertility and slow growth.
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