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There was no further increase in the number of internalised S. aureus up to 90 minutes, indicating that maximal invasion levels had been reached (Fig. 1).
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To determine whether maximal invasion of keratinocytes (FnBPR1 11 levels) could be triggered by over-expression of otherwise weakly-invasive FnBPR1 or FnBPR6 8 constructs, or whether invasion is absolutely dependent on multiple FnBRs within FnBPA, we employed a nisin-inducible system to control and over-express FnBPA variants on the surface of L. lactis [17].
Annual species were dominant in all invasion levels (Table 1).
The pH did not vary significantly (P > 0.05) between the invasion levels.
Similarly, the content of silt did not vary in both locations and invasion levels.
Clay was the dominant fraction of the soil in all invasion levels and both locations.
S. Typhimurium internalization is heavily dependant on actin-based membrane ruffles, however evidence presented here demonstrates that spectrin cytoskeletal components are also needed for maximal invasion.
Previous work has shown that a single high-affinity, or three low-affinity repeats were sufficient to trigger maximal invasion of endothelial cells [17].
Maximal invasion distance was determined by averaging 3 maximal distances for individual microtumors.
As shown in Figure 3, both BMS and BMECs are powerful invasion stimuli, possibly inducing maximal invasion within our assay system.
Our results support the findings that Erk 1/2 and p38 are necessary for maximal invasion by C. jejuni.
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