Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies (original) (raw)

• Horvitz, H.R. Worms, life, and death. Chembiochem 4, 697–711 (2003).
  Article CAS PubMed Google Scholar
• Danial, N.N. & Korsmeyer, S.J. Cell death: critical control points. Cell 116, 205–219 (2004).
  Article CAS PubMed Google Scholar
• Degterev, A., Boyce, M. & Yuan, J. A decade of caspases. Oncogene 22, 8543–8567 (2003).
  Article CAS PubMed Google Scholar
• Green, D.R. & Reed, J.C. Mitochondria and apoptosis. Science 281, 1309–1312 (1998).
  Article CAS PubMed Google Scholar
• Wang, X. The expanding role of mitochondria in apoptosis. Genes Dev. 15, 2922–2933 (2001).
  CAS PubMed Google Scholar
• Cory, S. & Adams, J.M. The Bcl2 family: regulators of the cellular life-or-death switch. Nature Rev. Cancer 2, 647–656 (2002).
  Article CAS Google Scholar
• Lindsten, T. et al. The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues. Mol. Cell 6, 1389–1399 (2000).
  Article CAS PubMed PubMed Central Google Scholar
• Wei, M.C. et al. Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death. Science 292, 727–730 (2001).
  Article CAS PubMed PubMed Central Google Scholar
• Hsu, Y.T., Wolter K.G. & Youle, R.J. Cytosol-to-membrane redistribution of Bax and Bcl-X(L) during apoptosis. Proc. Natl Acad. Sci. USA 94, 3668–3672 (1997).
  Article CAS PubMed PubMed Central Google Scholar
• Wei, M.C. et al. tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c. Genes Dev. 14, 2060–2071 (2000).
  CAS PubMed PubMed Central Google Scholar
• Cheng, E.H., Sheiko T.V., Fisher, J.K., Craigen, W.J. & Korsmeyer, S.J. VDAC2 inhibits BAK activation and mitochondrial apoptosis. Science 301, 513–517 (2003).
  Article CAS PubMed Google Scholar
• Antonsson, B., Montessuit, S., Sanchez, B. & Martinou, J.C. Bax is present as a high molecular weight oligomer/complex in the mitochondrial membrane of apoptotic cells. J. Biol. Chem. 276, 11615–11623 (2001).
  Article CAS PubMed Google Scholar
• Cheng, E.H. et al. BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis. Mol. Cell 8, 705–711 (2001).
  Article CAS PubMed Google Scholar
• Zong, W.X., Lindsten, T., Ross, A.J., MacGregor, G.R . & Thompson, C.B. BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak. Genes Dev. 15, 1481–1486 (2001).
  Article CAS PubMed PubMed Central Google Scholar
• Letai, A. et al. Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. Cancer Cell 2, 183–192 (2002).
  Article CAS PubMed Google Scholar
• Kuwana, T. et al. BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly. Mol. Cell 17, 525–535 (2005).
  Article CAS PubMed Google Scholar
• Chen, L. et al. Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. Mol. Cell 17, 393–403 (2005).
  Article CAS PubMed Google Scholar
• Li, H., Zhu, H., Xu, C.J. & Yuan, J. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Cell 94, 491–501 (1998).
  Article CAS PubMed Google Scholar
• Luo, X., Budihardjo, I., Zou, H., Slaughter, C. & Wang, X. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors. Cell 94, 481–490 (1998).
  Article CAS PubMed Google Scholar
• Cuconati, A., Mukherjee, C., Perez, D. & White, E. DNA damage response and MCL-1 destruction initiate apoptosis in adenovirus-infected cells. Genes Dev. 17, 2922–2932 (2003).
  Article CAS PubMed PubMed Central Google Scholar
• Willis, S.N. et al. Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins. Genes Dev. 19, 1294–1305 (2005).
  Article CAS PubMed PubMed Central Google Scholar
• Nijhawan, D. et al. Elimination of Mcl-1 is required for the initiation of apoptosis following ultraviolet irradiation. Genes Dev. 17, 1475–1486 (2003).
  Article CAS PubMed PubMed Central Google Scholar
• Opferman, J.T. et al. Development and maintenance of B and T lymphocytes requires antiapoptotic MCL-1. Nature 426, 671–676 (2003).
  Article CAS PubMed Google Scholar
• Inohara, N., Ding, L., Chen, S. & Nunez, G. harakiri, a novel regulator of cell death, encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L). EMBO J. 16, 1686–1694 (1997).
  Article CAS PubMed PubMed Central Google Scholar
• Puthalakath, H. et al. Bmf: a proapoptotic BH3-only protein regulated by interaction with the myosin V actin motor complex, activated by anoikis. Science 293, 1829–1832 (2001).
  Article CAS PubMed Google Scholar
• Terradillos, O., Montessuit, S., Huang, D.C. & Martinou, J.C. Direct addition of BimL to mitochondria does not lead to cytochrome c release. FEBS Lett. 522, 29–34 (2002).
• Cartron, P.F. et al. The first α-helix of Bax plays a necessary role in its ligand-induced activation by the BH3-only proteins Bid and PUMA. Mol. Cell 16, 807–818 (2004).
  Article CAS PubMed Google Scholar
• Chipuk, J.E., Bouchier-Hayes, L., Kuwana, T., Newmeyer, D.D. & Green, D.R. PUMA couples the nuclear and cytoplasmic proapoptotic function of p53. Science 309, 1732–1735 (2005).
  Article CAS PubMed Google Scholar
• Mihara, M. et al. p53 has a direct apoptogenic role at the mitochondria. Mol. Cell 11, 577–590 (2003).
  Article CAS PubMed Google Scholar
• Nakano, K. & Vousden, K.H. PUMA, a novel proapoptotic gene, is induced by p53. Mol. Cell 7, 683–694 (2001).
  Article CAS PubMed Google Scholar
• Li, C. et al. Bcl-X(L) affects Ca2+ homeostasis by altering expression of inositol 1,4,5-trisphosphate receptors. Proc. Natl Acad. Sci. USA 99, 9830–9835 (2002).
  Article CAS PubMed PubMed Central Google Scholar
• Scorrano, L. et al. BAX and BAK regulation of endoplasmic reticulum Ca2+: a control point for apoptosis. Science 300, 135–139 (2003).
  Article CAS PubMed Google Scholar
• Oda, E. et al. Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis. Science 288, 1053–1058 (2000).
  Article CAS PubMed Google Scholar
• Yu, J., Zhang, L., Hwang, P.M., Kinzler, K.W. & Vogelstein, B. PUMA induces the rapid apoptosis of colorectal cancer cells. Mol. Cell 7, 673–682 (2001).
  Article CAS PubMed Google Scholar
• Imaizumi, K. et al. Molecular cloning of a novel polypeptide, DP5, induced during programmed neuronal death. J. Biol. Chem. 272, 18842–18848 (1997).
  Article CAS PubMed Google Scholar
• Putcha, G.V. et al. Induction of BIM, a proapoptotic BH3-only BCL-2 family member, is critical for neuronal apoptosis. Neuron 29, 615–628 (2001).
  Article CAS PubMed Google Scholar
• Dijkers, P.F., Medema, R.H., Lammers, J.W., Koenderman, L. & Coffer, P.J. Expression of the pro-apoptotic Bcl-2 family member Bim is regulated by the forkhead transcription factor FKHR-L1. Curr. Biol. 10, 1201–1204 (2000).
  Article CAS PubMed Google Scholar
• Morrison, D.J., English, M.A. & Licht, J.D. WT1 induces apoptosis through transcriptional regulation of the proapoptotic Bcl-2 family member Bak. Cancer Res. 65, 8174–8182 (2005).
  Article CAS PubMed Google Scholar
• Yin, X.M. et al. _Bid_-deficient mice are resistant to Fas-induced hepatocellular apoptosis. Nature 400, 886–891 (1999).
  Article CAS PubMed Google Scholar
• Bouillet, P. et al. Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity. Science 286, 1735–1738 (1999).
  Article CAS PubMed Google Scholar
• Imaizumi, K. et al. Critical role for DP5/Harakiri, a Bcl-2 homology domain 3-only Bcl-2 family member, in axotomy-induced neuronal cell death. J. Neurosci. 24, 3721–3725 (2004).
  Article CAS PubMed PubMed Central Google Scholar
• Jeffers, J.R. et al. Puma is an essential mediator of p53-dependent and -independent apoptotic pathways. Cancer Cell 4, 321–328 (2003).
  Article CAS PubMed Google Scholar
• Villunger, A. et al. p53- and drug-induced apoptotic responses mediated by BH3-only proteins Puma and Noxa. Science 302, 1036–1038 (2003).
  Article CAS PubMed Google Scholar
• Shibue, T. et al. Integral role of Noxa in p53-mediated apoptotic response. Genes Dev. 17, 2233–2238 (2003).
  Article CAS PubMed PubMed Central Google Scholar
• Coultas, L. et al. Proapoptotic BH3-only Bcl-2 family member Bik/Blk/Nbk is expressed in hemopoietic and endothelial cells but is redundant for their programmed death. Mol. Cell Biol. 24, 1570–1581 (2004).
  Article CAS PubMed PubMed Central Google Scholar
• Ranger, A.M. et al. Bad-deficient mice develop diffuse large B cell lymphoma. Proc. Natl Acad. Sci. USA 100, 9324–9329 (2003).
  Article PubMed PubMed Central Google Scholar
• Bouillet, P., Cory, S., Zhang, L.C., Strasser, A. & Adams, J.M. Degenerative disorders caused by Bcl-2 deficiency prevented by loss of its BH3-only antagonist Bim. Dev. Cell 1, 645–653 (2001).
  Article CAS PubMed Google Scholar
• Walensky, L.D. et al. Activation of apoptosis in vivo by a hydrocarbon-stapled BH3 helix. Science 305, 1466–1470 (2004).
  Article CAS PubMed PubMed Central Google Scholar
• Oltersdorf, T. et al. An inhibitor of Bcl-2 family proteins induces regression of solid tumours. Nature 435, 677–681 (2005).
  Article CAS PubMed Google Scholar
• Harada, H., Quearry, B., Ruiz-Vela, A. & Korsmeyer, S.J. Survival factor-induced extracellular signal-regulated kinase phosphorylates BIM, inhibiting its association with BAX and proapoptotic activity. Proc. Natl Acad. Sci. USA 101, 15313–15317 (2004).
  Article CAS PubMed PubMed Central Google Scholar