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We infected WT, Nlrc4−/− and Tlr5−/− alveolar macrophages with LpWT or LpFlaA- and examined replication over 72 hours.
While the binding of Srs2 to sumoylated PCNA inhibits the recombination pathway, the binding of replicative polymerases stimulates replication over the lesion (Fig. 4).
Here we sought to understand how miR-122 inhibition influences HCV replication over time.
Here we set out to better understand how miR-122 inhibition influences HCV replication over time.
We give simulation results to show the performance of our algorithms, and to present the advantage of partial replication over full replication.
To further understand the increased effects of MAL on TV infection and replication, we monitored TV replication over the first 28 hours after inoculation of LLC-MK2 cells with or without MAL treatment.
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Once replication is over and the replication checkpoint is turned off, HR centers can be assembled to complete the repair of the accumulated ssDNA gaps and broken ends.
For example, DNA-repairing genes are turned off in cancer cells, while genes that promote replication are over-expressed.
These results were consistent across replications over three years using the same sample.
Difficulty in measuring small growth increments with traditional methods results in large measurement errors requiring many replications over long time spans.
Forages were grown in a complete randomized block design with 3 replications over a two year period, harvested at the milk stage (MS) and dough stage (DS).
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