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PMID:9241272
| Citation |
Knudson, CM and Korsmeyer, SJ (1997) Bcl-2 and Bax function independently to regulate cell death. Nat. Genet. 16:358-63 |
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| Abstract |
The BCL-2 family has various pairs of antagonist and agonist proteins that regulate apoptosis. Whether their function is interdependent is uncertain. Using a genetic approach to address this question, we utilized gain- and loss-of-function models of Bcl-2 and Bax and found that apoptosis and thymic hypoplasia characteristic of Bcl-2-deficient mice are largely absent in mice also deficient in Bax. A single copy of Bax promoted apoptosis in the absence of Bcl-2. In contrast, overexpression of Bcl-2 still repressed apoptosis in the absence of Bax. While an in vivo competition exists between Bax and Bcl-2, each is able to regulate apoptosis independently. |
| Links |
PubMed Online version:10.1038/ng0897-358 |
| Keywords |
Animals; Apoptosis/physiology; Cell Cycle; Cricetinae; Gene Deletion; Humans; Mice; Mice, Knockout; Phenotype; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins/physiology; Proto-Oncogene Proteins c-bcl-2/genetics; Proto-Oncogene Proteins c-bcl-2/physiology; Rabbits; bcl-2-Associated X Protein |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
References
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