Molecular characterization of mitochondrial apoptosis-inducing factor

@article{Susin1999MolecularCO,
  title={Molecular characterization of mitochondrial apoptosis-inducing factor},
  author={Santos A. Susin and Hans K Lorenzo and Naoufal Zamzami and Isabel Marzo and Bryan E. Snow and Greg M Brothers and Joan Mangion and Etienne Daniel Jacotot and Paola Costantini and Markus Loeffler and Nathanael Larochette and David R. Goodlett and Ruedi Aebersold and D. Siderovski and Josef M. Penninger and Guido Kroemer},
  journal={Nature},
  year={1999},
  volume={397},
  pages={441-446}
}
Mitochondria play a key part in the regulation of apoptosis (cell death). Their intermembrane space contains several proteins that are liberated through the outer membrane in order to participate in the degradation phase of apoptosis. Here we report the identification and cloning of an apoptosis-inducing factor, AIF, which is sufficient to induce apoptosis of isolated nuclei. AIF is a flavoprotein of relative molecular mass 57,000 which shares homology with the bacterial oxidoreductases; it is… 
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The precise mode of action and importance of cytochrome c in apoptosis in mammalian cells has become clear through biochemical, structural and genetic studies, and more recently identified factors, for example HtrA2/OMI and Smac/DIABLO, are still being studied intensively in order to delineate their functions in apoptoses.
Mitochondrio‐nuclear translocation of AIF in apoptosis and necrosis
  • E. Daugas, S. Susin, G. Kroemer
  • Biology
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2000
TLDR
Data are compatible with the hypothesis that AIF is a caspase‐independent mitochondrial death effector responsible for partial chromatinolysis, and in conditions of ATP depletion, AIF translocation correlates with the appearance of large‐scale DNA fragmentation.
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The discovery of the previously overlooked COX-AIFM12 complex and clues provided by the structural model hint at potential roles of AIFM1 in oxidative phosphorylation biogenesis and in programmed cell death.
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The main goal of this project was to investigate the involvement of mitochondria in cell death and reveal a novel role for the HCN2 channel in cellDeath signaling and uncover a new potential therapeutic drug target.
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