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. 2005 Jan;79(2):1084–1098. doi: 10.1128/JVI.79.2.1084-1098.2005

FIG. 8.

FIG. 8.

Localization of F1L to the mitochondria is necessary for apoptosis inhibition. (A) HeLa cells were transfected with either pEGFP or pEGFP-F1Lwt for 16 h and treated with 10 ng of TNF-α/ml for 5, 8, 10, or 15 h. Loss of the inner mitochondrial membrane potential was assessed by TMRE fluorescence in EGFP-positive cells by two-color flow cytometry. Standard deviations were calculated from three ormore independent experiments. (B) HeLa cells were transfected with either pEGFP, pEGFP-F1Lwt, pEGFP-Bcl-2, pEGFP-F1LHTR (1-218), pEGFP-F1LTR (1-206), pEGFP-F1Ltail(+) (206-226), pEGFPtail(-) (207-226), or pEGFP-F1LCyb5 for 16 h and treated with 10 ng of TNF-α/ml for 8 h. Loss of the inner mitochondrial membrane potential was assessed by TMRE fluorescence in EGFP-positive cells by two-color flow cytometry. Standard deviations were calculated from three or more independent experiments. (C) F1LCyb5 localizes to the ER. HeLa cells were transfected with PEGFP-F1LCyb5 (a and d) and stained with either Mitotracker Red (b) or ER-Tracker (e). Merge images indicate that EGFP-F1LCyb5 localized to the ER (f) but not mitochondria (c). (D) Expression levels of various F1L constructs. HeLa cells were transfected, and protein levels were determined by Western blotting with anti-EGFP.