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- Wei-Xing Zong
- 1Department of Medicine, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104
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- Chi Li
- 1Department of Medicine, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104
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- Georgia Hatzivassiliou
- 1Department of Medicine, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104
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- Tullia Lindsten
- 2Department of Pathology and Laboratory Medicine, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104
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- Qian-Chun Yu
- 2Department of Pathology and Laboratory Medicine, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104
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- Junying Yuan
- 3Department of Cell Biology, Harvard Medical School, Boston, MA 02115
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- Craig B. Thompson
- 1Department of Medicine, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104
書誌事項
- 公開日
- 2003-07-07
- DOI
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- 10.1083/jcb.200302084
- 公開者
- Rockefeller University Press
この論文をさがす
説明
<jats:p>Bax and Bak play a redundant but essential role in apoptosis initiated by the mitochondrial release of apoptogenic factors. In addition to their presence at the mitochondrial outer membrane, Bax and Bak can also localize to the ER. Agents that initiate ER stress responses can induce conformational changes and oligomerization of Bax on the ER as well as on mitochondria. In wild-type cells, this is associated with caspase 12 cleavage that is abolished in bax−/−bak−/− cells. In bax−/−bak−/− cells, introduction of Bak mutants selectively targeted to either mitochondria or the ER can induce apoptosis. However, ER-targeted, but not mitochondria-targeted, Bak leads to progressive depletion of ER Ca2+ and induces caspase 12 cleavage. In contrast, mitochondria-targeted Bak leads to enhanced caspase 7 and PARP cleavage in comparison with the ER-targeted Bak. These findings demonstrate that in addition to their functions at mitochondria, Bax and Bak also localize to the ER and function to initiate a parallel pathway of caspase activation and apoptosis.</jats:p>
収録刊行物
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- The Journal of Cell Biology
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The Journal of Cell Biology 162 (1), 59-69, 2003-07-07
Rockefeller University Press