The Bcl-2 protein family.

[1]  J. Martinou,et al.  Bid Induces the Oligomerization and Insertion of Bax into the Outer Mitochondrial Membrane , 2000, Molecular and Cellular Biology.

[2]  J. Martinou,et al.  Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria. , 2000, The Biochemical journal.

[3]  A. Strasser,et al.  Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity. , 1999, Science.

[4]  S. Korsmeyer,et al.  Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis , 1999, Nature.

[5]  J C Reed,et al.  Ion Channel Activity of the BH3 Only Bcl-2 Family Member, BID* , 1999, The Journal of Biological Chemistry.

[6]  Masashi Narita,et al.  Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC , 1999, Nature.

[7]  Susan S. Taylor,et al.  Phosphorylation and inactivation of BAD by mitochondria-anchored protein kinase A. , 1999, Molecular cell.

[8]  Jean-Claude Martinou,et al.  Bid-induced Conformational Change of Bax Is Responsible for Mitochondrial Cytochrome c Release during Apoptosis , 1999, The Journal of cell biology.

[9]  J. Martinou,et al.  The Release of Cytochrome c from Mitochondria during Apoptosis of NGF-deprived Sympathetic Neurons Is a Reversible Event , 1999, The Journal of cell biology.

[10]  S. Korsmeyer,et al.  Solution Structure of the Proapoptotic Molecule BID A Structural Basis for Apoptotic Agonists and Antagonists , 1999, Cell.

[11]  Junying Yuan,et al.  Solution Structure of BID, an Intracellular Amplifier of Apoptotic Signaling , 1999, Cell.

[12]  C. Print,et al.  Apoptosis regulator bcl-w is essential for spermatogenesis but appears otherwise redundant. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[13]  Jean-Claude Martinou,et al.  Bax-induced Cytochrome C Release from Mitochondria Is Independent of the Permeability Transition Pore but Highly Dependent on Mg2+ Ions , 1998, The Journal of cell biology.

[14]  J C Reed,et al.  Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis. , 1998, Science.

[15]  Junying Yuan,et al.  Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis , 1998, Cell.

[16]  S. Patel,et al.  Purification and biochemical properties of soluble recombinant human Bax. , 1998, Protein expression and purification.

[17]  J C Reed,et al.  Bax directly induces release of cytochrome c from isolated mitochondria. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[18]  G. Kroemer,et al.  The Permeability Transition Pore Complex: A Target for Apoptosis Regulation by Caspases and Bcl-2–related Proteins , 1998, The Journal of experimental medicine.

[19]  G. Núñez,et al.  Mtd, a Novel Bcl-2 Family Member Activates Apoptosis in the Absence of Heterodimerization with Bcl-2 and Bcl-XL * , 1998, The Journal of Biological Chemistry.

[20]  C. Borner,et al.  Alphaviruses induce apoptosis in Bcl‐2‐overexpressing cells: evidence for a caspase‐mediated, proteolytic inactivation of Bcl‐2 , 1998, The EMBO journal.

[21]  M. Skinner,et al.  Testicular degeneration in Bclw-deficient mice , 1998, Nature Genetics.

[22]  Y. Tsujimoto,et al.  Bcl-2 prevents apoptotic mitochondrial dysfunction by regulating proton flux. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[23]  S. Cory,et al.  The conserved N‐terminal BH4 domain of Bcl‐2 homologues is essential for inhibition of apoptosis and interaction with CED‐4 , 1998, The EMBO journal.

[24]  John Calvin Reed,et al.  The Mitochondrial F0F1-ATPase proton pump is required for function of the proapoptotic protein Bax in yeast and mammalian cells. , 1998, Molecular cell.

[25]  C. Borner,et al.  Bcl-2 prolongs cell survival after Bax-induced release of cytochrome c , 1998, Nature.

[26]  A. Strasser,et al.  Bim: a novel member of the Bcl‐2 family that promotes apoptosis , 1998, The EMBO journal.

[27]  E. Cheng,et al.  Conversion of Bcl-2 to a Bax-like death effector by caspases. , 1997, Science.

[28]  S. Srinivasula,et al.  Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade , 1997, Cell.

[29]  A. Hsueh,et al.  Bok is a pro-apoptotic Bcl-2 protein with restricted expression in reproductive tissues and heterodimerizes with selective anti-apoptotic Bcl-2 family members. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[30]  S. Korsmeyer,et al.  Apoptosis-associated signaling pathways are required for chemotherapy-mediated female germ cell destruction , 1997, Nature Medicine.

[31]  L. Peso,et al.  Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt. , 1997, Science.

[32]  S. R. Datta,et al.  Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death Machinery , 1997, Cell.

[33]  M. Muda,et al.  Bcl-2 Undergoes Phosphorylation by c-Jun N-terminal Kinase/Stress-activated Protein Kinases in the Presence of the Constitutively Active GTP-binding Protein Rac1* , 1997, The Journal of Biological Chemistry.

[34]  S. Korsmeyer,et al.  BH3 Domain of BAD Is Required for Heterodimerization with BCL-XL and Pro-apoptotic Activity* , 1997, The Journal of Biological Chemistry.

[35]  P. Paty,et al.  Mitochondrial Proliferation and Paradoxical Membrane Depolarization during Terminal Differentiation and Apoptosis in a Human Colon Carcinoma Cell Line , 1997, The Journal of cell biology.

[36]  F Gambale,et al.  Inhibition of Bax channel-forming activity by Bcl-2. , 1997, Science.

[37]  John Calvin Reed.  Double identity for proteins of the Bcl-2 family , 1997, Nature.

[38]  J C Reed,et al.  Channel formation by antiapoptotic protein Bcl-2. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[39]  F. Shibasaki,et al.  Suppression of signalling through transcription factor NF-AT by interactions between calcineurin and Bcl-2 , 1997, Nature.

[40]  Y. Hsu,et al.  Cytosol-to-membrane redistribution of Bax and Bcl-X(L) during apoptosis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[41]  S. Fesik,et al.  Identification of a novel regulatory domain in Bcl‐xL and Bcl‐2 , 1997, The EMBO journal.

[42]  Andy J. Minn,et al.  Bcl-xL forms an ion channel in synthetic lipid membranes , 1997, Nature.

[43]  Elizabeth Yang,et al.  Serine Phosphorylation of Death Agonist BAD in Response to Survival Factor Results in Binding to 14-3-3 Not BCL-XL , 1996, Cell.

[44]  C. Milliman,et al.  BID: a novel BH3 domain-only death agonist. , 1996, Genes & development.

[45]  G. Kroemer,et al.  Bcl-2 inhibits the mitochondrial release of an apoptogenic protease , 1996, The Journal of experimental medicine.

[46]  S. Korsmeyer,et al.  BAX Is Required for Neuronal Death after Trophic Factor Deprivation and during Development , 1996, Neuron.

[47]  R. Meadows,et al.  X-ray and NMR structure of human Bcl-xL, an inhibitor of programmed cell death , 1996, Nature.

[48]  J. Hunter,et al.  A Peptide Sequence from Bax That Converts Bcl-2 into an Activator of Apoptosis (*) , 1996, The Journal of Biological Chemistry.

[49]  C. Croce,et al.  Taxol induces bcl-2 phosphorylation and death of prostate cancer cells. , 1996, Cancer research.

[50]  E. Cheng,et al.  Bax-independent inhibition of apoptosis by Bcl-XL , 1996, Nature.

[51]  S. Farrow,et al.  New members of the Bcl-2 family and their protein partners. , 1996, Current opinion in genetics & development.

[52]  T. Chittenden,et al.  A conserved domain in Bak, distinct from BH1 and BH2, mediates cell death and protein binding functions. , 1995, The EMBO journal.

[53]  al. et,et al.  Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice , 1995, Science.

[54]  C. Borner,et al.  Dissection of functional domains in Bcl-2 alpha by site-directed mutagenesis. , 1994, Biochemistry and cell biology = Biochimie et biologie cellulaire.

[55]  D. Newmeyer,et al.  Cell-free apoptosis in Xenopus egg extracts: Inhibition by Bcl-2 and requirement for an organelle fraction enriched in mitochondria , 1994, Cell.

[56]  Jean-Claude Martinou,et al.  Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia , 1994, Neuron.

[57]  S. Krajewski,et al.  Apoptosis regulation by interaction of Bcl-2 protein and Raf-1 kinase. , 1994, Oncogene.

[58]  P. Bernardi,et al.  Regulation of the permeability transition pore, a voltage-dependent mitochondrial channel inhibited by cyclosporin A. , 1994, Biochimica et biophysica acta.

[59]  C. Borner,et al.  The protein bcl-2 alpha does not require membrane attachment, but two conserved domains to suppress apoptosis , 1994, The Journal of cell biology.

[60]  Z. Oltvai,et al.  BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax , 1994, Nature.

[61]  D. Bredesen,et al.  Bcl-2 inhibition of neural death: decreased generation of reactive oxygen species. , 1993, Science.

[62]  S. Korsmeyer,et al.  Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair , 1993, Cell.

[63]  Z. Oltvai,et al.  Bcl-2 functions in an antioxidant pathway to prevent apoptosis , 1993, Cell.

[64]  John Calvin Reed,et al.  Investigation of the subcellular distribution of the bcl-2 oncoprotein: residence in the nuclear envelope, endoplasmic reticulum, and outer mitochondrial membranes. , 1993, Cancer research.

[65]  A. Halestrap,et al.  Inhibition of Ca2(+)-induced large-amplitude swelling of liver and heart mitochondria by cyclosporin is probably caused by the inhibitor binding to mitochondrial-matrix peptidyl-prolyl cis-trans isomerase and preventing it interacting with the adenine nucleotide translocase. , 1990, The Biochemical journal.

[66]  Y. Tsujimoto,et al.  Involvement of the bcl-2 gene in human follicular lymphoma. , 1985, Science.

[67]  D. Green,et al.  Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD‐specific caspase activation and independently of mitochondrial transmembrane depolarization , 1998, The EMBO journal.

[68]  J. Dichgans,et al.  Taxol-mediated augmentation of CD95 ligand-induced apoptosis of human malignant glioma cells: association with bcl-2 phosphorylation but neither activation of p53 nor G2/M cell cycle arrest. , 1998, British Journal of Cancer.