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In studies of mice, cells with the invasive form of Mena were better able to recognize and crawl toward higher concentrations of fibronectin, moving along the collagen pathways, while cells without MenaINV did not move toward the higher concentrations.
This indicates that, after endogenous TCRα rearrangement in TCR transgenic mice, cells with new TCRs composed of transgenic TCRβ chain and endogenous TCRα chains develop in a similar pathway as they do in normal mice.
In V1 of rl−/− mice, cells with different laminar fates are present at all cortical depths.
Therefore, it is unknown whether, in heterogeneous tumors in living mice, cells with high metastatic potential can transfer biomaterial to less metastatic cells, thereby influencing tumor progression.
To address these questions, McCormack et al. infected human and mice cells with bacteria that cause serious diseases of the digestive tract.
In the PTEN mutant mice, cells with ectopic dendrites exhibit an increase in pAKT and phosphorylated GSK3β, whereas cells without ectopic dendrites have no pAKT changes.
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Computational analysis of such data sets allows for accurate (∼99.5%) reconstruction of chromosome-spanning haplotypes for ∼95% of alleles in hybrid mouse cells with 30× sequencing coverage.
To demonstrate the functional conservation of pathways, five were tested in Drosophila and mouse cells, with each pathway responding to alkylation damage in both species.
To test this theory, they mixed virus-infected mouse cells with T lymphocytes from other infected mice.
The researchers then treated mouse cells with thousands of compounds and picked out the ones that made the cells glow.
We have studied HIV-1 replication in primary mouse T cells and compared the efficiency of each step in mouse cells with that in primary human T cells.
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