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. Author manuscript; available in PMC: 2014 Sep 11.
Published in final edited form as: Cell Host Microbe. 2013 Sep 11;14(3):281–293. doi: 10.1016/j.chom.2013.08.002

Figure 1. Disrupting host cell endocytic machinery impacts both enteroviral replication and cellular cholesterol landscape.

Figure 1

(A) CVB3 replication when CME components are depleted. Mean peak replication data +/−SEM, from 2 independent experiments with 6 replicates each was normalized with respect to cell viability and plotted as % of non-target siRNA treated cells. **: p<0.01

(B) PV and CVB3 replication when caveolins are depleted. Mean peak replication data +/−SEM from 2 independent experiments with 6 replicates each was normalized with respect to cell viability and plotted as % of non-target siRNA treated cells. **: p<0.01

(C) Plasma membrane cholesterol is stored in lipid droplets when CME components are depleted. Scale bar 5µm.

(D) Quantification of lipid droplets immunolabeled with anti-ADRP. Mean data +/−SEM from n=50 cells for each siRNA treatment is plotted.

(E) Steady state esterified cholesterol levels when CME components are depleted. Mean data +/− SEM of 3 independent experiments for each siRNA.

(F) Steady state free and esterified cholesterol levels when caveolins are depleted. Mean data +/− SEM of 3 independent experiments for each siRNA.

(G) Free cholesterol distribution when Cav 2 is depleted. Free cholesterol is labeled with filipin. Scale bar 5µm.

Figure 1 related to Figure S1 and Table S1.