Journal
DEVELOPMENTAL CELL
Volume 2, Issue 1, Pages 55-67Publisher
CELL PRESS
DOI: 10.1016/S1534-5807(01)00116-2
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Funding
- NATIONAL CANCER INSTITUTE [R01CA050239, R37CA050239] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [P41RR001219] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [T32HL007627] Funding Source: NIH RePORTER
- NCI NIH HHS [CA50239-14] Funding Source: Medline
- NCRR NIH HHS [P41 RR001219, RR01219] Funding Source: Medline
- NHLBI NIH HHS [T32-HL07627-16] Funding Source: Medline
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The mechanism during apoptosis by which cytochrome c is rapidly and completely released in the absence of mitochondrial swelling is uncertain. Here, we show that two distinct pathways are involved. One mediates release of cytochrome c across the outer mitochondrial membrane, and another, characterized in this study, is responsible for the redistribution of cytochrome c stored in intramitochondrial cristae. We have found that the BH3-only molecule tBID induces a striking remodeling of mitochondrial structure with mobilization of the cytochrome c stores (similar to85%) in cristae. This reorganization does not require tBID's BH3 domain and is independent of BAK, but is inhibited by CsA. During this process, individual cristae become fused and the junctions between the cristae and the intermembrane space are opened.
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