By Peter J. Quinn (Editor), Valerian E. Kagan (Editor)
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Extra resources for Phospholipid Metabolism in Apoptosis (Subcellular Biochemistry, Volume 36) (Subcellular Biochemistry)
1999, Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC, Nature 399: 483-487. , 1999a, Molecular characterization of mitochondrial apaptosis-inducing factor, Nature 397: 441-446. M. , 1999b Mitochondrial release of caspase-2 and –9 during the apoptotic process, J. Exp. Med. 189: 381-393. , 1998, Caspases: enemies within, Science 281: 13121316. , 2000, Susceptibility to drug-induced apoptosis correlates with differential modulation of Bad, Bcl-2 and protein levels, Cell Death and Differentiation 7: 574-586.
We have proposed that peroxidation of cardiolipin may result in a discharge of cytochrome c due to a weakening of the interaction between the lipid and the protein. Our proposed mechanism is outlined in Figure 6, with a tentative assumption that once the acyl chains of cardiolipin are peroxidized, their hydrophobicity will diminish and a resulting conformational change cannot be accommodated within the cavity between the heme plane and the inner surface of cytochrome c. Our model of cytochrome c release during apoptosis is not an alternative mechanism to the Bid/Bax-regulated release of cytochrome c.
It was found that when higher doses of the drug was employed necrosis of the cells resulted. 3 Phospholipid probes The dynamics of lipid movement between the two leaflets of membrane lipid bilayers has been monitored using a variety of phospholipid analogs. Most of the analogs incorporate a reporter group attached to the C-2 of the glycerol moiety. One common substituent is a florescent-labelled fatty acid to form 1,2-(palmitoyl-N-4-nitrobenzo-2-oxa-1,3-diazole-amino-caproyl) phosphatidylserine (NBD-PS) (Martin and Pagano, 1987).