Fig. 1: Caspase-8 is activated after HSV-1 infection and required for HSV-1-induced caspase-3 activation and apoptosis in MEFs. | Cell Death & Differentiation

Fig. 1: Caspase-8 is activated after HSV-1 infection and required for HSV-1-induced caspase-3 activation and apoptosis in MEFs.

From: Caspase-8 is required for HSV-1-induced apoptosis and promotes effective viral particle release via autophagy inhibition

Fig. 1

A Caspase-8 (IETDase) activity assay of total extracts of wild-type (wt) MEFs infected with 10 m.o.i. of HSV-1 for 0 to 36 h. Results are presented as relative fluorescence units (RFU). B Anti-caspase-8 western blot analysis of total extracts of MEFs infected with HSV-1 for 0, 8, 14 and 24 h, showing the inactive p55 caspase-8 pro-form and the cleaved, active p43/p41 and p18/p10 forms. The right line shows an extract from caspase-8−/− MEFs. C Percentage of FITC-Annexin-V/7-AAD-negative (surviving) wt and caspase-8−/− (Casp-8−/−) MEFs infected with HSV-1 for 0 (NT), 24, 48 and 72 h. D Anti-caspase-3 western blot analysis of total extracts of wt and caspase-8−/− MEFs infected with HSV-1 for 8, 14 and 24 h showing the inactive p32 caspase-3 pro-form and the cleaved, active p17 form. Data in A and C represent the means of 3–6 independent experiments ± SD. Statistical evaluation by one-way ANOVA: **p < 0.01; ***p < 0.001. In B and D, β-actin served as a loading control.

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