... of flSIRT1 (top) and 75SIRT1 (bottom). See text for details. To determine cytochrome C (CytoC) binding to flSIRT1 and 75SIRT1, we used a hypothetic structural analysis via PyMOL software. Despite their identical sequences, the superimposition of the structures of flSIRT1 and 75SIRT1 revealed a root...

... determinants of cell fate. Bcl-2 proteins Ceramide transfer protein Cytochrome c Endoplasmic reticulum Membrane contact sites Mitochondrial apoptosis VAP receptor Seventh Framework Programme 10.13039/501100004963 289278 Deutsche Forschungsgemeinschaft 10.13039/501100001659...

...Lydia Lartigue; Chantal Medina; Laura Schembri; Paul Chabert; Marion Zanese; Flora Tomasello; Renée Dalibart; Didier Thoraval; Marc Crouzet; François Ichas; Francesca De Giorgi Bax is considered to be pivotal in inducing cytochrome c release (CCR) from mitochondria during apoptosis. Indeed, Bax...

...Changhui Wang; Guo-Lei Zhou; Srilakshmi Vedantam; Peng Li; Jeffrey Field Mitochondria play a central role in regulating apoptosis by releasing proapoptotic contents such as cytochrome c , and generating reactive oxygen species (ROS). Early in apoptosis, proteins translocate to mitochondria...

..., at stage III, Bax and Bak began to form small complexes at the MOM. Later, at stage IV, these Bax and Bak complexes expanded to become large clusters. We found that the formation of Bax-Bak small complexes at stage III was responsible for permeabilizing the MOM to release cytochrome c and Smac. Using...

...Kieran Gillick; Martin Crompton Truncated Bid (tBid) releases cytochrome c from mitochondria by inducing Bak (and Bax) pore formation in the outer membrane. An important issue is whether a second tBid action, independent of Bak and Bax, is also required to enhance cytochrome c mobility...

... and caspase activators. Despite this, studies in Caenorhabditis elegans , Drosophila and vertebrates have revealed some apparent differences both in the way apoptosis is regulated and in the way individual molecules contribute to the propagation of the death signal. For example, whereas cytochrome c released...

... nitric oxide synthase (iNOS) expression and produced equal amounts of nitrite, which ruled out attenuated iNOS activity during P35-mediated protection. Rather, expression of P35 inhibited translocation of mitochondrial cytochrome c into cytosol, mitochondrial depolarization, activation of caspase-9...

... interaction between the Hsp and its target (+). (e-mail: [email protected] ) © The Company of Biologists Limited 2004 2004 Heat shock protein (Hsp) Co-chaperones Apoptosis Apoptosome Caspases Death receptor Mitochondria Proteasome NF-κB Cytochrome c Bcl-2 Paradoxically...

... mitochondrial dysfunction and cell death. * Author for correspondence (e-mail: [email protected] ) © The Company of Biologists Limited 2003 2003 Bcl-2 Endoplasmic reticulum ER Mitochondria Bcl-Cb5 Calcium BH3-only Cytochrome c Apoptosis is a cellular process by which a cell...

...Wenhua Gao; Yongmei Pu; Kathy Q. Luo; Donald C. Chang During apoptosis, cytochrome c is released from mitochondria to the cytosol to activate a caspase cascade, which commits the cell to the death process. It has been proposed that the release of cytochrome c is caused by a swelling...

... in the mitochondria. It also inhibited glucose deprivation-induced cytochrome c release from the mitochondria. It is possible that overexpression of Bcl2 prevents glucose deprivation-induced ceramide generation, probably by preventing the leakage of hydroperoxide from the mitochondria. We also observed that glucose...