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Science 292 (5517): 727-730

Copyright © 2001 by the American Association for the Advancement of Science

Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death

Michael C. Wei,12* Wei-Xing Zong,3* Emily H.-Y. Cheng,1 Tullia Lindsten,3 Vily Panoutsakopoulou,1 Andrea J. Ross,4 Kevin A. Roth,5 Grant R. MacGregor,4 Craig B. Thompson,3dagger Stanley J. Korsmeyer1dagger

Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of a "BH3-domain-only" BCL-2 family member, triggers the homooligomerization of "multidomain" conserved proapoptotic family members BAK or BAX, resulting in the release of cytochrome c from mitochondria. We find that cells lacking both Bax and Bak, but not cells lacking only one of these components, are completely resistant to tBID-induced cytochrome c release and apoptosis. Moreover, doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin. Thus, activation of a "multidomain" proapoptotic member, BAX or BAK, appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli.

1 Howard Hughes Medical Institute, Departments of Pathology and Medicine, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
2 Division of Biology and Biomedical Sciences, Washington University School of Medicine, St. Louis, MO 63110, USA.
3 Departments of Medicine and Pathology and Laboratory Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
4 Center for Molecular Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
5 Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.
*   These authors contributed equally to this work.

dagger    To whom correspondence should be addressed. E-mail: craig{at}; stanley_korsmeyer{at}

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The HIV-1-Specific Protein Casp8p41 Induces Death of Infected Cells through Bax/Bak.
A. M. Sainski, S. Natesampillai, N. W. Cummins, G. D. Bren, J. Taylor, D. T. Saenz, E. M. Poeschla, and A. D. Badley (2011)
J. Virol. 85, 7965-7975
   Abstract »    Full Text »    PDF »
Q. Ma, H. Fang, W. Shang, L. Liu, Z. Xu, T. Ye, X. Wang, M. Zheng, Q. Chen, and H. Cheng (2011)
J. Biol. Chem. 286, 27573-27581
   Abstract »    Full Text »    PDF »
BRCA1 Loss Induces GADD153-Mediated Doxorubicin Resistance in Prostate Cancer.
P. De Luca, E. S. Vazquez, C. P. Moiola, F. Zalazar, J. Cotignola, G. Gueron, K. Gardner, and A. De Siervi (2011)
Mol. Cancer Res. 9, 1078-1090
   Abstract »    Full Text »    PDF »
Tonight, the same old, deadly programme: BH3-only proteins, mitochondria and yeast.
B. Oettinghaus, S. Frank, and L. Scorrano (2011)
EMBO J. 30, 2754-2756
   Abstract »    Full Text »    PDF »
Squamous Cell Carcinoma Antigen 1 Promotes Caspase-8-Mediated Apoptosis in Response to Endoplasmic Reticulum Stress While Inhibiting Necrosis Induced by Lysosomal Injury.
E. Ullman, J.-A. Pan, and W.-X. Zong (2011)
Mol. Cell. Biol. 31, 2902-2919
   Abstract »    Full Text »    PDF »
Transient binding of an activator BH3 domain to the Bak BH3-binding groove initiates Bak oligomerization.
H. Dai, A. Smith, X. W. Meng, P. A. Schneider, Y.-P. Pang, and S. H. Kaufmann (2011)
J. Cell Biol. 194, 39-48
   Abstract »    Full Text »    PDF »
Ammonia-induced autophagy is independent of ULK1/ULK2 kinases.
H. Cheong, T. Lindsten, J. Wu, C. Lu, and C. B. Thompson (2011)
PNAS 108, 11121-11126
   Abstract »    Full Text »    PDF »
UV irradiation resistance-associated gene suppresses apoptosis by interfering with BAX activation.
X. Yin, L. Cao, R. Kang, M. Yang, Z. Wang, Y. Peng, Y. Tan, L. Liu, M. Xie, Y. Zhao, et al. (2011)
EMBO Rep. 12, 727-734
   Abstract »    Full Text »    PDF »
Cannabinoid receptor 1 mediates high glucose-induced apoptosis via endoplasmic reticulum stress in primary cultured rat mesangial cells.
J. C. Lim, S. K. Lim, M. J. Park, G. Y. Kim, H. J. Han, and S. H. Park (2011)
Am J Physiol Renal Physiol 301, F179-F188
   Abstract »    Full Text »    PDF »
Tubular network formation protects mitochondria from autophagosomal degradation during nutrient starvation.
A. S. Rambold, B. Kostelecky, N. Elia, and J. Lippincott-Schwartz (2011)
PNAS 108, 10190-10195
   Abstract »    Full Text »    PDF »
Ischemic preconditioning attenuates mitochondrial localization of PTEN induced by ischemia-reperfusion.
L. Zu, X. Zheng, B. Wang, N. Parajuli, C. Steenbergen, L. C. Becker, and Z. P. Cai (2011)
Am J Physiol Heart Circ Physiol 300, H2177-H2186
   Abstract »    Full Text »    PDF »

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