14-3-3 Interacts Directly with and Negatively Regulates Pro-apoptotic Bax*
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Masashi Narita | Hikaru Matsuda | Shigeomi Shimizu | T. Sugiyama | M. Narita | Y. Tsujimoto | S. Shimizu | M. Nomura | Toshinori Ito | H. Matsuda | Toshinori Ito | Tomoyasu Sugiyama | Yoshihide Tsujimoto | Masaya Nomura | Masaya Nomura
[1] S. Cory,et al. The Bcl-2 protein family: arbiters of cell survival. , 1998, Science.
[2] L. Romer,et al. Integrin-Mediated Survival Signals Regulate the Apoptotic Function of Bax through Its Conformation and Subcellular Localization , 2000, The Journal of cell biology.
[3] S. Masters,et al. 14-3-3 Proteins Mediate an Essential Anti-apoptotic Signal* , 2001, The Journal of Biological Chemistry.
[4] Masashi Narita,et al. Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC , 1999, Nature.
[5] Y. Hsu,et al. Conformation of the Bax C‐terminus regulates subcellular location and cell death , 1999, The EMBO journal.
[6] 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.
[7] S. Masters,et al. Interaction of 14-3-3 with a nonphosphorylated protein ligand, exoenzyme S of Pseudomonas aeruginosa. , 1999, Biochemistry.
[8] S. Korsmeyer,et al. Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis , 1998, The EMBO journal.
[9] 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.
[10] Junying Yuan,et al. Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis , 1998, Cell.
[11] A. Strasser,et al. The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex. , 1999, Molecular cell.
[12] Robert L Moritz,et al. Identification of DIABLO, a Mammalian Protein that Promotes Apoptosis by Binding to and Antagonizing IAP Proteins , 2000, Cell.
[13] Yamamura Ken-ichi,et al. Efficient selection for high-expression transfectants with a novel eukaryotic vector , 1991 .
[14] 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.
[15] R. Liddington,et al. Crystal structure of the zeta isoform of the 14-3-3 protein , 1995, Nature.
[16] P. Allen,et al. Interaction of 14-3-3 with Signaling Proteins Is Mediated by the Recognition of Phosphoserine , 1996, Cell.
[17] D. Green,et al. Apoptosis: Letting Slip The Dogs Of War , 2002, Current Biology.
[18] J. Martinou,et al. Bax Is Present as a High Molecular Weight Oligomer/Complex in the Mitochondrial Membrane of Apoptotic Cells* , 2001, The Journal of Biological Chemistry.
[19] S. Kawabata,et al. cDNA cloning and characterization of mitochondrial import stimulation factor (MSF) purified from rat liver cytosol. , 1994, Journal of biochemistry.
[20] Xiaodong Wang,et al. Bid, a Bcl2 Interacting Protein, Mediates Cytochrome c Release from Mitochondria in Response to Activation of Cell Surface Death Receptors , 1998, Cell.
[21] T. Chittenden,et al. Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[22] Xiaodong Wang,et al. Smac, a Mitochondrial Protein that Promotes Cytochrome c–Dependent Caspase Activation by Eliminating IAP Inhibition , 2000, Cell.
[23] K. Muegge,et al. Withdrawal of IL-7 induces Bax translocation from cytosol to mitochondria through a rise in intracellular pH. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[24] S. Srinivasula,et al. Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade , 1997, Cell.
[25] H. Fu,et al. Suppression of apoptosis signal-regulating kinase 1-induced cell death by 14-3-3 proteins. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[26] S. Smerdon,et al. Structure of a 14-3-3 protein and implications for coordination of multiple signalling pathways , 1995, Nature.
[27] J C Reed,et al. Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD. , 1999, Science.
[28] J C Reed,et al. Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis. , 1998, Science.
[29] Yi-Te Hsu,et al. Movement of Bax from the Cytosol to Mitochondria during Apoptosis , 1997, The Journal of cell biology.
[30] B. Verdoodt,et al. The G2/M Regulator 14-3-3ς Prevents Apoptosis through Sequestration of Bax* , 2001, The Journal of Biological Chemistry.
[31] Xiaodong Wang,et al. Apaf-1, a Human Protein Homologous to C. elegans CED-4, Participates in Cytochrome c–Dependent Activation of Caspase-3 , 1997, Cell.
[32] Andreas Villunger,et al. Bmf: A Proapoptotic BH3-Only Protein Regulated by Interaction with the Myosin V Actin Motor Complex, Activated by Anoikis , 2001, Science.
[33] Jean-Claude Martinou,et al. Breaking the mitochondrial barrier , 2001, Nature Reviews Molecular Cell Biology.
[34] A. Aitken. 14-3-3 and its possible role in co-ordinating multiple signalling pathways. , 1996, Trends in cell biology.
[35] T. Isobe,et al. Identification of the Site of Interaction of the 14-3-3 Protein with Phosphorylated Tryptophan Hydroxylase (*) , 1995, The Journal of Biological Chemistry.
[36] S. Korsmeyer,et al. Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death , 2001, Science.
[37] Roger Y. Tsien,et al. Changes in intramitochondrial and cytosolic pH: early events that modulate caspase activation during apoptosis , 2000, Nature Cell Biology.
[38] M. Narita,et al. Apoptotic cytosol facilitates Bax translocation to mitochondria that involves cytosolic factor regulated by Bcl-2. , 1999, Cancer research.
[39] 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.
[40] A. Strasser,et al. Keeping killers on a tight leash: transcriptional and post-translational control of the pro-apoptotic activity of BH3-only proteins , 2002, Cell Death and Differentiation.
[41] Y. Hsu,et al. Nonionic Detergents Induce Dimerization among Members of the Bcl-2 Family* , 1997, The Journal of Biological Chemistry.
[42] M. Greenberg,et al. Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor , 1999, Cell.
[43] 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.
[44] S. Korsmeyer,et al. Regulated Targeting of BAX to Mitochondria , 1998, The Journal of cell biology.
[45] 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.
[46] Shigeomi Shimizu,et al. Bcl‐2 family: Life‐or‐death switch , 2000, FEBS letters.
[47] T. Isobe,et al. The 14‐3‐3 protein binds its target proteins with a common site located towards the C‐terminus , 1997, FEBS letters.