作者: Marco Tafani , Natalie O. Karpinich , Ada Serroni , Matteo A. Russo , John L. Farber
DOI: 10.1002/JCP.20691
关键词: Cyclosporin a 、 Jurkat cells 、 Mitochondrion 、 Biology 、 Cell 、 Cell culture 、 Cell killing 、 Apoptosis 、 Cell biology 、 Cytosol 、 Clinical biochemistry 、 Physiology
摘要: Cyclosporin A (CyA) and bongkrekic acid (BK) prevented Fas-induced apoptosis in two type I cell lines (H9 SKW6.4) II (Jurkat CEM). CyA BK inhibited the release of cytochrome c all four lines. In cells CEM cells, did not prevent translocation Bax to mitochondria. these same full-length Bid decreased mitochondria cytosol. The cleavage product Bid, tBid, appeared cytosol a lesser extent Jurkat also cytosol, but increased Similar other tBid H9 SKW6.4 caspase-8 inhibitor Z-Ile-Glu(OMe)-Thr-Asp(OMe)-CH2F (IETD) killing. IETD Bax, degradation accumulation tBid. By contrast, only marginally protected cells. presence IETD, translocated mitochondria, absence any or produced depletion ATP, an effect that occur It is concluded extrinsic signaling pathway mitochondrial dependent as intrinsic J. Cell. Physiol. 208: 556–565, 2006. © 2006 Wiley-Liss, Inc.