Mitochondrial membrane dynamics, cristae remodelling and apoptosis Export

@article{citeulike:776561, abstract = {Mitochondria form a highly dynamic reticular network in living cells, and undergo continuous fusion/fission events and changes in ultrastructural architecture. Although significant progress has been made in elucidating the molecular events underlying these processes, their relevance to normal cell function remains largely unexplored. Emerging evidence, however, suggests an important role for mitochondrial dynamics in cellular apoptosis. The mitochondria is at the core of the intrinsic apoptosis pathway, and provides a reservoir for protein factors that induce caspase activation and chromosome fragmentation. Additionally, mitochondria modulate Ca2+ homeostasis and are a source of various metabolites, including reactive oxygen species, that have the potential to function as second messengers in response to apoptotic stimuli. One of the mitochondrial factors required for activation of caspases in most intrinsic apoptotic pathways, cytochrome c, is largely sequestered within the intracristae compartment, and must migrate into the boundary intermembrane space in order to allow passage across the outer membrane to the cytosol. Recent evidence argues that inner mitochondrial membrane dynamics regulate this process. Here, we review the contribution of mitochondrial dynamics to the intrinsic apoptosis pathway, with emphasis on the inner membrane.}, author = {Heath-Engel, Hannah M. and Shore, Gordon C.}, booktitle = {Mitochondrial Dynamics in Cell Life and Death}, citeulike-article-id = {776561}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.bbamcr.2006.02.006}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/16574258}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=16574258}, citeulike-linkout-3 = {http://www.sciencedirect.com/science/article/B6T20-4JG4BT1-1/2/72bf8508c5b832b5e499f5166e84bb99}, doi = {10.1016/j.bbamcr.2006.02.006}, journal = {Biochimica et Biophysica Acta (BBA) - Molecular Cell Research}, keywords = {biology, mitochondria}, month = {}, number = {5-6}, pages = {549--560}, posted-at = {2006-07-27 19:30:37}, priority = {0}, title = {Mitochondrial membrane dynamics, cristae remodelling and apoptosis}, url = {http://dx.doi.org/10.1016/j.bbamcr.2006.02.006}, volume = {1763}, year = {2006} }

TY - JOUR ID - citeulike:776561 L3 - citeulike-article-id:776561 N2 - Mitochondria form a highly dynamic reticular network in living cells, and undergo continuous fusion/fission events and changes in ultrastructural architecture. Although significant progress has been made in elucidating the molecular events underlying these processes, their relevance to normal cell function remains largely unexplored. Emerging evidence, however, suggests an important role for mitochondrial dynamics in cellular apoptosis. The mitochondria is at the core of the intrinsic apoptosis pathway, and provides a reservoir for protein factors that induce caspase activation and chromosome fragmentation. Additionally, mitochondria modulate Ca2+ homeostasis and are a source of various metabolites, including reactive oxygen species, that have the potential to function as second messengers in response to apoptotic stimuli. One of the mitochondrial factors required for activation of caspases in most intrinsic apoptotic pathways, cytochrome c, is largely sequestered within the intracristae compartment, and must migrate into the boundary intermembrane space in order to allow passage across the outer membrane to the cytosol. Recent evidence argues that inner mitochondrial membrane dynamics regulate this process. Here, we review the contribution of mitochondrial dynamics to the intrinsic apoptosis pathway, with emphasis on the inner membrane. IS - 5-6 JF - Biochimica et Biophysica Acta (BBA) - Molecular Cell Research EP - 560 TI - Mitochondrial membrane dynamics, cristae remodelling and apoptosis VL - 1763 T2 - Mitochondrial Dynamics in Cell Life and Death SP - 549 KW - biology KW - mitochondria AU - Heath-Engel, Hannah AU - Shore, Gordon PY - 2006/0// UR - http://dx.doi.org/10.1016/j.bbamcr.2006.02.006 ER -