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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.

Mouse cells with a deletion of the Ledgf (Psip1) gene have been engineered and show a pronounced defect in lentiviral infection and no effect on retroviral infection [36].

To determine how this retention related to the oxidative stress of 20% O2, we treated PRE mouse cells with H2O2, a strong oxidant.

The significance of successfully infecting mouse cells with HCMV is that doing so would enable the development of an HCMV mouse model.

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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In order to exclude the involvement of polioviruses L20B-cells (transgenic mouse cell with the human poliovirus receptor) were also used for virus cultivation.

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.

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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