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The mice in the study were inoculated with human cells because mouse cells do not become infected with H.I.V.
They stop growing at a third the density that the mouse cells do.
Instead of arresting their growth at a low density, the cells now grew into thick clusters, just as cancer-prone mouse cells do.
Mouse cells do not have a Trim5α ortholog, but other related proteins may be involved in this host restriction.
These findings support the idea that biological activities of the mouse and human SASPs are conserved, and that mouse cells do not express a SASP when the senesce (arrest growth) in 20% O2.
While SIRT6-deficient mouse cells do not show impaired resolution of DSBs, human S6KD cells do demonstrate such a defect.
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PRE mouse cells did not significantly stimulate the growth of EpH4-v derived tumors; this was also true for mBFs that senesced after passage in 20% O2 [SEN(OXI)] (Figs. 7A C, S6A).
These results indicate that the presence of <10% mouse cells does not significantly skew human gene expression signatures.
The model was further tested with experimental mixtures of human and mouse cells, demonstrating that the presence of mouse cells does not significantly skew expression profiles when xenografts contain 90% or more human cells.
Additionally, Table 1 shows that when mouse and human cells were damaged in S phase, allowed to recover for 72 hours and then analyzed for their cell cycle position, human cells tended to arrest in G2 while mouse cells did not.
Mouse ES cells do not readily differentiate into the trophectoderm.
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CEO of Professional Science Editing for Scientists @ prosciediting.com