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Role of Bax and Bak in mitochondrial morphogenesis.

Authors
Karbowski, M; Norris, KL; Cleland, MM; Jeong, SY; Youle, RJ
Citation
Nature, 443(7112):658-662, 2006
Journal Title
Nature
ISSN
0028-08361476-4687
Abstract
Bcl-2 family proteins are potent regulators of programmed cell death. Although their intracellular localization to mitochondria and the endoplasmic reticulum has focused research on these organelles, how they function remains unknown. Two members of the Bcl-2 family, Bax and Bak, change intracellular location early in the promotion of apoptosis to concentrate in focal clusters at sites of mitochondrial division. Here we report that in healthy cells Bax or Bak is required for normal fusion of mitochondria into elongated tubules. Bax seems to induce mitochondrial fusion by activating assembly of the large GTPase Mfn2 and changing its submitochondrial distribution and membrane mobility-properties that correlate with different GTP-bound states of Mfn2. Our results show that Bax and Bak regulate mitochondrial dynamics in healthy cells and indicate that Bcl-2 family members may also regulate apoptosis through organelle morphogenesis machineries.
MeSH terms
AnimalsBiological TransportCells, CulturedGTP Phosphohydrolases/geneticsGTP Phosphohydrolases/metabolismGene ExpressionMiceMitochondria/physiology*Morphogenesisbcl-2 Homologous Antagonist-Killer Protein/metabolism*bcl-2-Associated X Protein/geneticsbcl-2-Associated X Protein/metabolism*
DOI
10.1038/nature05111
PMID
17035996
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Medical Genetics
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