RVFV Cell Signaling Figure 5. Comparison of RPMA and Western blot data. Left panels (A) show the RPMA data. Right panels (B) show Western blot confirmatory data. X axis labels, time post infection (h.p.i.); Y axis labels, protein level relative to untreated cells (%) at 0 h.p.i. Open triangles, closed triangles and open squares correspond to the low MOI, high MOI and uninfected cells, respectively. RPMA data represent mean values and confidence intervals of two-tail t-test (a = 0.05, n = 3). Western blot data represent average of two independent experiments. doi:10.1371/journal.pone.0013805.g005 dephosphorylation at MOI of 0.002, while JNK1/2 phosphorylation continued to increase at MOI of 0.0002 (Table 1 and Fig. 4, 5). The p38 MAPK pathway can be activated in response to a plethora of inflammatory cytokines, as well as pathogens and by environmental stress, such as osmotic stress, ultraviolet light, heat shock, and hypoxia. The activation of the p38 MAPK pathway is required for apoptosis induction in several different cellular models [20–23]. Additionally, stress-elicited p38 activation was shown to cause G2/M cell cycle arrest and to regulate the cell cycle through modulation of p53 and p73 tumor suppressor proteins [24,25]. Similar to the proteins from Group II (Table 1, Fig. 4, 5), RVFV infection in HSAECs stimulated phosphorylation of p38 on T180. The activation pattern of MAPKs prompted us to analyze the phosphorylation of transcriptional factors as their most important PLoS ONE | www.plosone.org 8 November 2010 | Volume 5 | Issue 11 | e13805