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Apoptosis Initiated When BH3 Ligands Engage Multiple Bcl-2 Homologs, Not Bax or Bak
Abstract
A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2–like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak.
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Metadata
- Authors
- Willis, S. N., Fletcher, J. I., Kaufmann, T., van Delft, M. F., Chen, L., Czabotar, P. E., Ierino, H., Lee, E. F., Fairlie, W. D., Bouillet, P., Strasser, A., Kluck, R. M., Adams, J. M., & Huang, D. C. S.
- Venue
- Science
- Published
- 2007-02-09
- Volume
- 315
- Issue
- 5813
- Pages
- 856-859
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2008841394
- Cited by
- 1,125
- References
- 5
- FWCI
- 53.76
- Type
- journal article
- Language
- en
- Open access
- closed
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