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. 2010 Dec 23;1:137. doi: 10.3389/fmicb.2010.00137

Figure 3.

Figure 3

Kinase and phosphatase antagonists reversibly inhibit PV formation and C. burnetii growth. HeLa cells were infected with C. burnetii for 48 h in the presence of the indicated kinase inhibitors, then inhibitors were removed from cells for an additional 48 h. At 48 h post-washout, cells were processed for fluorescence microscopy using anti-CD63 antibody (green) to detect PV and anti-C. burnetii antibody (red) to detect bacteria. DAPI was used to stain host and bacterial DNA (blue). Following washout, CD63-positive PV formed in cells previously treated with PRL1 (pentamidine), PKC (GF 109203X), PKA (H-89), or MLCK (ML-7) inhibitors, indicating these kinases are involved in PV formation and are not directly toxic to C. burnetii. In contrast, washout of KN-93 did not allow PV expansion or bacterial replication, indicating the effects of this inhibitor are not reversible. Control = infected, untreated cells.