Mitochondrial fission in apoptosis

By R. Youle, M. Karbowski. Nature reviews. Molecular cell biology, 2005

811 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/86d50233e75af84ac5553d2671803f9177ffb24c

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Citations in the corpus

OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion. (2006, neutral): “Given its function in mitochondrial fusion, one could predict that OPA1 protects by counteracting apoptotic fragmentation of mitochondria, a process observed in several paradigms of cell death (Youle and Karbowski, 2005).”
Calcium and apoptosis: ER-mitochondria Ca2+ transfer in the control of apoptosis (2008, background): “Similarly, stimulation of organelle fission (by DRP1 overexpression or Mfn1/2 and OPA1 inhibition) promotes apoptosis by facilitating cytochrome c release and apoptosome assembly (Youle and Karbowski, 2005).”
Mitochondrial fusion, fission and autophagy as a quality control axis: the bioenergetic view. (2008, background): “Detailed reviews on the molecular machinery of mitochondrial fusion and fission, protein turnover and autophagy are available in the these references [8,31–36].”
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).”
Mff is an essential factor for mitochondrial recruitment of Drp1 during mitochondrial fission in mammalian cells (2010, background): “Mitochondria undergo extensive fragmentation early during apoptosis, and Drp1 is essential for the normal progression of apoptosis (Youle and Karbowski, 2005; Parone and Martinou, 2006; Arnoult 2007; Suen et al., 2008; Ishihara et al., 2009).”
Mitochondrial rhomboid PARL regulates cytochrome c release during apoptosis via OPA1-dependent cristae remodeling. (2006, background): “Parl Is Dispensable for Mitochondrial Fusion The yeast ortholog of Parl, RBD1, is required for mainte- nance of mitochondrial morphology, which in turn influ- ences mitochondrial participation to apoptosis (Youle and Karbowski, 2005).”