The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis
Open accessAbstract
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.
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Cites
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Noxa, a BH3-Only Member of the Bcl-2 Family and Candidate Mediator of p53-Induced Apoptosis
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Cytochrome c Deficiency Causes Embryonic Lethality and Attenuates Stress-Induced Apoptosis
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Metadata
- Authors
- Zong, W.-X., Li, C., Hatzivassiliou, G., Lindsten, T., Yu, Q.-C., Yuan, J., & Thompson, C. B.
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2003-07-07
- Volume
- 162
- Issue
- 1
- Pages
- 59-69
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W1996952569
- Cited by
- 595
- References
- 7
- FWCI
- 15.98
- Type
- journal article
- Language
- en
- Open access
- green
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- Zong, W.-X., Li, C., Hatzivassiliou, G., Lindsten, T., Yu, Q.-C., Yuan, J., & Thompson, C. B. (2003). Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis. The Journal of Cell Biology. https://doi.org/10.1083/jcb.200302084
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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