Fig. 1.

Plasmodium LS development is differentially impacted by host-targeted kinase inhibitors. a Schematic representing work flow to identify host kinases involved in LS infection by kinase profiling and elastic net regression. b P. falciparum GFP-Luciferase expressing blood stage parasites were cultured at 2% parasitemia in 5% hematocrit and evaluated for growth in response to 37 kinase inhibitors at 44 h.p.i. Light output was used as a surrogate measurement for parasite biomass. Values are normalized to the light output of non-treated parasites, which is indicated by a solid line. Kinase inhibitors that exhibited toxicity against blood stage parasites were removed for subsequent study (depicted in red). Data is the average of three independent experiments. c 150,000 Hepa 1–6 cells were infected with 50,000 P. yoelii parasites and then treated with kinase inhibitors at 500 nM 1.5 h.p.i. P. yoelii LS development in the presence of kinase inhibitors was evaluated by microscopy at 24 h.p.i. All values are normalized to vehicle-treated control (indicated by a solid line). Kinase inhibitors that exhibited high variability in parasite clearance were excluded from downstream analysis (depicted in green). Data shown is the average of 3–4 independent experiments. Error bars represent standard deviation of independent experiments. Individual data points are provided in Supplementary Table 1