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Joel G.R. Weaver, Agathe Tarze, Tia C. Moffat, Morgane LeBras, Aurelien Deniaud, Catherine Brenner, Gary D. Bren, Mario Y. Morin, Barbara N. Phenix, Li Dong, Susan X. Jiang, Valerie L. Sim, Bogdan Zurakowski, Jessica Lallier, Heather Hardin, Peter Wettstein, Rolf P.G. van Heeswijk, Andre Douen, Romano T. Kroemer, Sheng T. Hou, Steffany A.L. Bennett, David H. Lynch, Guido Kroemer, Andrew D. Badley
Published in Volume 115, Issue 7
J Clin Invest. 2005; 115(7):1828–1838 doi:10.1172/JCI22954
Abstract | Full text | PDF
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Figure 4

NFV blocks Bax-induced apoptosis but not Bax activation. (A) Mouse liver mitochondria were incubated with 10 μM of NFV followed by 1 μM Vpr-derived peptide, 0.5 mM ATR, or 4 μM Bax while absorption was assessed at 545 nm. The loss of absorption induced by 0.5 mM ATR within 20 minutes was considered at 100% of large amplitude swelling. All experiments were reproduced 3 times. (B) Jurkat T cells were treated with an agonistic anti-Fas antibody in the presence or absence of NFV and stained with Hoechst 33342 for nuclear morphology, an antibody (or isotype control) specific for activated Bax, and an Alexa Fluor–conjugated secondary antibody. All cells were stained with Hoechst and varying combinations of NFV or DMSO, CH-11, and anti-Bax or isotype antibody as indicated. (C) Jurkat T cells were transfected with Bax, and immediately following transfection, NFV or control was added and ΔΨm was assessed.