A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis.

By L. Scorrano, M. Ashiya, K. Buttle, S. Weiler, Scott A Oakes, C. Mannella, S. Korsmeyer. Developmental Cell, 2002

1,057 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/93d0c017f998002bb56ac76be340825f8c84bf28

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Citations in the corpus

Making heads or tails of phospholipids in mitochondria (2011, background): “Ups1 was originally identified to affect the processing of the dynaminlike GTPase Mgm1 in yeast (Sesaki et al., 2006) and later shown to regulate CL level in mitochondria (Osman et al., 2009a; Tamura et al., 2009).”
The BCL-2 Family Reunion (2010, background): “Nevertheless, in the absence Molecular Cell 37, February 12, 2010 ª2010 Elsevier Inc. 305 of caspase activation, cristae junctions undergo subtle but significant changes that may be BAK and BAX independent and regulated by cyclosporine A (Scorrano et al., 2002; Yamaguchi et al., 2008).”
Cytochrome c: functions beyond respiration (2008, background): “, it has been suggested that cristae are remodelled such that cytochrome c is redistributed in the mitochondria prior to translocation through the OM”
Mitochondrial dynamics and apoptosis. (2008, background): “Therefore, since the bulk of the cytochrome c seems to be localized within cristae in healthy cells, it has been suggested that complete cytochrome c release from the mitochondria cannot occur without cristae remodeling (Scorrano et al. 2002).”
Apoptosis: A Review of Programmed Cell Death (2007, background): “Cytochrome c release from the mitochondria can also be assayed using fluorescence and electron microscopy in living or fixed cells (Scorrano et al., 2002).”
Cytochrome c acts as a cardiolipin oxygenase required for release of proapoptotic factors (2005, methodology): “To address this, we performed measurements of peroxidase activity and electron-transport (succinate oxidase) activity in liver mitochondria before and after treatment with alamethicin, known to permeabilize mitochondrial membranes and remodel cristae to remove loosely (electrostatically) bound cyt ”
Tubular network formation protects mitochondria from autophagosomal degradation during nutrient starvation (2011, background): “Changes in mitochondrial cristae and mitochondrial fragmentation, for example, play a vital role in apoptosis (16, 17).”
Mitochondrial dynamics in mammalian health and disease. (2009, background): “Importantly, not only does the formation of distinct types of pores regulate this release, but the morphology of mitochondrial cristae also plays a relevant role, as it controls the compartmentalization of some of these mitochondrial cell-death effectors and, therefore, their release to the cytosol ”
Bcl-2-family proteins and the role of mitochondria in apoptosis. (2003, background): “In this regard, one might ask whether the Bid-induced changes in mitochondrial ultrastructure observed by Korsmeyer and colleagues [83] could in fact have been a response to Ca2þ that was somehow potentiated by Bid.”