The Bcl-2-regulated apoptotic pathway

Apoptosis (programmed cell death) is required for the removal of infected, damaged or unwanted cells and its disrupted regulation is implicated in cancer, autoimmunity and degenerative disorders. At the molecular level, multiple signaling pathways converge on a family of cysteine proteases (caspases

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

[2]  S. Cory,et al.  Bcl-2 family members do not inhibit apoptosis by binding the caspase activator Apaf-1. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[3]  David L. Vaux,et al.  Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells , 1988, Nature.

[4]  K. Lei,et al.  JNK phosphorylation of Bim-related members of the Bcl2 family induces Bax-dependent apoptosis , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[5]  S. Frank,et al.  Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosis , 2002, The Journal of cell biology.

[6]  C. Borner,et al.  Characterization of the signal that directs Bcl-xL, but not Bcl-2, to the mitochondrial outer membrane , 2003, The Journal of cell biology.

[7]  M. Lackmann,et al.  The structure of Bcl‐w reveals a role for the C‐terminal residues in modulating biological activity , 2003, The EMBO journal.

[8]  Jean-Claude Martinou,et al.  Bax oligomerization in mitochondrial membranes requires tBid (caspase-8-cleaved Bid) and a mitochondrial protein. , 2002, The Biochemical journal.

[9]  W. Zong,et al.  BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak. , 2001, Genes & development.

[10]  R. Youle,et al.  Bax and Bak Coalesce into Novel Mitochondria-Associated Clusters during Apoptosis , 2001, The Journal of cell biology.

[11]  K. Vousden,et al.  PUMA, a novel proapoptotic gene, is induced by p53. , 2001, Molecular cell.

[12]  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.

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

[14]  Wenhua Gao,et al.  Elimination of Mcl-1 is required for the initiation of apoptosis following ultraviolet irradiation. , 2003, Genes & development.

[15]  S. Korsmeyer,et al.  Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. , 2002, Cancer cell.

[16]  K. Gehring,et al.  Solution Structure of Human BCL-w , 2003, Journal of Biological Chemistry.

[17]  V. Mootha,et al.  tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c. , 2000, Genes & development.

[18]  Nico Tjandra,et al.  Structure of Bax Coregulation of Dimer Formation and Intracellular Localization , 2000, Cell.

[19]  A. Strasser,et al.  Apoptosis signaling. , 2000, Annual review of biochemistry.

[20]  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.

[21]  A. Strasser,et al.  BH3-Only Proteins—Essential Initiators of Apoptotic Cell Death , 2000, Cell.

[22]  S. Korsmeyer,et al.  BCL-2 family members and the mitochondria in apoptosis. , 1999, Genes & development.

[23]  Jean-Claude Martinou,et al.  Breaking the mitochondrial barrier , 2001, Nature Reviews Molecular Cell Biology.

[24]  H. Horvitz,et al.  The TRA-1A Sex Determination Protein of C. elegans Regulates Sexually Dimorphic Cell Deaths by Repressing the egl-1 Cell Death Activator Gene , 1999, Cell.

[25]  S. Cory,et al.  The Bcl2 family: regulators of the cellular life-or-death switch , 2002, Nature Reviews Cancer.

[26]  Mason R. Mackey,et al.  Bid, Bax, and Lipids Cooperate to Form Supramolecular Openings in the Outer Mitochondrial Membrane , 2002, Cell.

[27]  A. Petros,et al.  Rationale for Bcl‐XL/Bad peptide complex formation from structure, mutagenesis, and biophysical studies , 2000, Protein science : a publication of the Protein Society.

[28]  H. Horvitz,et al.  C. elegans cell survival gene ced-9 encodes a functional homolog of the mammalian proto-oncogene bcl-2 , 1994, Cell.

[29]  R. Meadows,et al.  Structure of Bcl-xL-Bak Peptide Complex: Recognition Between Regulators of Apoptosis , 1997, Science.

[30]  Keisuke Kuida,et al.  Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome , 2002, Nature.

[31]  C. Borner The Bcl-2 protein family: sensors and checkpoints for life-or-death decisions. , 2003, Molecular immunology.

[32]  Suzanne Cory,et al.  The Bcl-2 family: roles in cell survival and oncogenesis , 2003, Oncogene.

[33]  John Calvin Reed,et al.  Humanin peptide suppresses apoptosis by interfering with Bax activation , 2003, Nature.

[34]  S. Korsmeyer,et al.  BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis. , 2001, Molecular cell.

[35]  Tullio Pozzan,et al.  BAX and BAK Regulation of Endoplasmic Reticulum Ca2+: A Control Point for Apoptosis , 2003, Science.

[36]  H. Horvitz,et al.  Genetic control of programmed cell death in the nematode Caenorhabditis elegans. , 1999, Cancer research.

[37]  S. Korsmeyer,et al.  The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues. , 2000, Molecular cell.

[38]  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.