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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.
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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.
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).
While SIRT6-deficient mouse cells do not show impaired resolution of DSBs, human S6KD cells do demonstrate such a defect.
Using the whole transcript platform, our results show that mouse cells do not significantly skew cancer expression profiles when xenografts contain 90% or more human cells.
First, we stably transfected L cells, which like all mouse cells do not possess a MICA gene, with expression constructs encoding a MICA-129Met or MICA-129Val variant.
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