Bak1

Summary

Gene Symbol: Bak1
Description: BCL2-antagonist/killer 1
Alias: Bak, N-BAK1, N-Bak, bcl-2 homologous antagonist/killer, Bcl2 homologous antagonist/killer, apoptosis regulator BAK
Species: mouse

Top Publications

  1. pmc Stepwise activation of BAX and BAK by tBID, BIM, and PUMA initiates mitochondrial apoptosis
    Hyungjin Kim
    Molecular Oncology, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
    Mol Cell 36:487-99. 2009
  2. doi Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation
    James E Vince
    Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland
    Immunity 36:215-27. 2012
  3. pmc Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis
    Wei Xing Zong
    Department of Cancer Biology, Abramson Cancer Center, 421 Curie Blvd, BRB II III, 445, Philadelphia, PA 19104 6160, USA
    J Cell Biol 162:59-69. 2003
  4. ncbi A Bax/Bak-independent mechanism of cytochrome c release
    Takeshi Mizuta
    Laboratory of Molecular Genetics, Department of Medical Genetics, Osaka University Medical School, Osaka 565 0871, Japan
    J Biol Chem 282:16623-30. 2007
  5. pmc Proapoptotic BAX and BAK regulate the type 1 inositol trisphosphate receptor and calcium leak from the endoplasmic reticulum
    Scott A Oakes
    Howard Hughes Medical Institute, Dana Farber Cancer Institute, Brigham and Women s Hospital, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:105-10. 2005
  6. pmc Oligomerization of BAK by p53 utilizes conserved residues of the p53 DNA binding domain
    E Christine Pietsch
    Division of Medical Sciences and Program in Biomolecular Structure and Function, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA
    J Biol Chem 283:21294-304. 2008
  7. pmc Sequential activation of poly(ADP-ribose) polymerase 1, calpains, and Bax is essential in apoptosis-inducing factor-mediated programmed necrosis
    Rana S Moubarak
    Apoptose et Systeme Immunitaire, CNRS URA 1961, Institut Pasteur, 25 rue du Dr Roux, 75015 Paris, France
    Mol Cell Biol 27:4844-62. 2007
  8. pmc Bax targeting to mitochondria occurs via both tail anchor-dependent and -independent mechanisms
    A J Valentijn
    Wellcome Trust Centre for Cell Matrix Research, Faculty of Life Sciences, The University of Manchester, Manchester, UK
    Cell Death Differ 15:1243-54. 2008
  9. pmc Pseudomonas exotoxin A-mediated apoptosis is Bak dependent and preceded by the degradation of Mcl-1
    Xing Du
    Laboratory of Molecular Biology, National Cancer Institute, 37 Convent Drive, Bethesda, MD 20892 4264, USA
    Mol Cell Biol 30:3444-52. 2010
  10. ncbi BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development
    Yihru Fannjiang
    Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Dev Cell 4:575-85. 2003

Research Grants

Scientific Experts

Detail Information

Publications120 found, 100 shown here

  1. pmc Stepwise activation of BAX and BAK by tBID, BIM, and PUMA initiates mitochondrial apoptosis
    Hyungjin Kim
    Molecular Oncology, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
    Mol Cell 36:487-99. 2009
    While activation of BAX/BAK by BH3-only molecules (BH3s) is essential for mitochondrial apoptosis, the underlying mechanisms remain unsettled...
  2. doi Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation
    James E Vince
    Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland
    Immunity 36:215-27. 2012
    ....
  3. pmc Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis
    Wei Xing Zong
    Department of Cancer Biology, Abramson Cancer Center, 421 Curie Blvd, BRB II III, 445, Philadelphia, PA 19104 6160, USA
    J Cell Biol 162:59-69. 2003
    Bax and Bak play a redundant but essential role in apoptosis initiated by the mitochondrial release of apoptogenic factors. In addition to their presence at the mitochondrial outer membrane, Bax and Bak can also localize to the ER...
  4. ncbi A Bax/Bak-independent mechanism of cytochrome c release
    Takeshi Mizuta
    Laboratory of Molecular Genetics, Department of Medical Genetics, Osaka University Medical School, Osaka 565 0871, Japan
    J Biol Chem 282:16623-30. 2007
    Bax and Bak are multidomain pro-apoptotic members of the Bcl-2 family of proteins that regulate mitochondria-mediated apoptosis by direct modulation of mitochondrial membrane permeability...
  5. pmc Proapoptotic BAX and BAK regulate the type 1 inositol trisphosphate receptor and calcium leak from the endoplasmic reticulum
    Scott A Oakes
    Howard Hughes Medical Institute, Dana Farber Cancer Institute, Brigham and Women s Hospital, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:105-10. 2005
    Proapoptotic BCL-2 family members BAX and BAK are required for the initiation of mitochondrial dysfunction during apoptosis and for maintaining the endoplasmic reticulum (ER) Ca(2+) stores necessary for Ca(2+)-dependent cell death...
  6. pmc Oligomerization of BAK by p53 utilizes conserved residues of the p53 DNA binding domain
    E Christine Pietsch
    Division of Medical Sciences and Program in Biomolecular Structure and Function, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA
    J Biol Chem 283:21294-304. 2008
    ..Using immunopurification protocols and mass spectrometry, we previously identified the proapoptotic protein BAK as a mitochondrial p53-binding protein and showed that recombinant p53 directly binds to BAK and can induce its ..
  7. pmc Sequential activation of poly(ADP-ribose) polymerase 1, calpains, and Bax is essential in apoptosis-inducing factor-mediated programmed necrosis
    Rana S Moubarak
    Apoptose et Systeme Immunitaire, CNRS URA 1961, Institut Pasteur, 25 rue du Dr Roux, 75015 Paris, France
    Mol Cell Biol 27:4844-62. 2007
    ..Importantly, single ablation of the proapoptotic Bcl-2 family member Bax, but not Bak, prevented both AIF release and alkylating DNA damage-induced death...
  8. pmc Bax targeting to mitochondria occurs via both tail anchor-dependent and -independent mechanisms
    A J Valentijn
    Wellcome Trust Centre for Cell Matrix Research, Faculty of Life Sciences, The University of Manchester, Manchester, UK
    Cell Death Differ 15:1243-54. 2008
    Bax is a member of the Bcl-2 family that, together with Bak, is required for permeabilisation of the outer mitochondrial membrane (OMM)...
  9. pmc Pseudomonas exotoxin A-mediated apoptosis is Bak dependent and preceded by the degradation of Mcl-1
    Xing Du
    Laboratory of Molecular Biology, National Cancer Institute, 37 Convent Drive, Bethesda, MD 20892 4264, USA
    Mol Cell Biol 30:3444-52. 2010
    ..Here, we utilized mouse embryo fibroblasts (MEFs) deficient in Bak and Bax to determine the roles of these proteins in cell death induced by PE...
  10. ncbi BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development
    Yihru Fannjiang
    Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Dev Cell 4:575-85. 2003
    b>BAK is a pro-apoptotic BCL-2 family protein that localizes to mitochondria...
  11. pmc Intrinsic and extrinsic pathway signaling during neuronal apoptosis: lessons from the analysis of mutant mice
    Girish V Putcha
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Cell Biol 157:441-53. 2002
    ..proteins did not, however, exhibit functional redundancy or compensatory expression, at least in the Bax-/-, Bak-/-, Bim-/-, Bid-/-, and Bad-/- neurons examined...
  12. pmc Vaccinia virus F1L interacts with Bak using highly divergent Bcl-2 homology domains and replaces the function of Mcl-1
    Stephanie Campbell
    Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
    J Biol Chem 285:4695-708. 2010
    ..Despite this, F1L inhibits cytochrome c release from mitochondria by preventing Bak and Bax activation...
  13. ncbi BAX and BAK regulation of endoplasmic reticulum Ca2+: a control point for apoptosis
    Luca Scorrano
    Howard Hughes Medical Institute, Dana Farber Cancer Institute, Brigham and Women s Hospital, Department of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA
    Science 300:135-9. 2003
    BAX and BAK are "multidomain" proapoptotic proteins that initiate mitochondrial dysfunction but also localize to the endoplasmic reticulum (ER)...
  14. ncbi Role of Bax and Bak in mitochondrial morphogenesis
    Mariusz Karbowski
    Biochemistry Section, SNB, NINDS, NIH, Bethesda, Maryland 20892, USA
    Nature 443:658-62. 2006
    ..Two members of the Bcl-2 family, Bax and Bak, change intracellular location early in the promotion of apoptosis to concentrate in focal clusters at sites of ..
  15. pmc A conserved domain in Bak, distinct from BH1 and BH2, mediates cell death and protein binding functions
    T Chittenden
    Apoptosis Technology, Inc, Cambridge, MA 02139, USA
    EMBO J 14:5589-96. 1995
    ..The Bcl-2 homolog, Bak, promotes apoptosis and binds anti-apoptotic family members including Bcl-2 and Bcl-xL...
  16. ncbi Gene structure, cDNA sequence, and expression of murine Bak, a proapoptotic Bcl-2 family member
    E Ulrich
    Imperial Cancer Research Fund, 44 Lincoln s Inn Fields, London, WC2A 3PX, United Kingdom
    Genomics 44:195-200. 1997
    To facilitate the creation of Bak knockout mice and the further analysis of this Bcl-2 family member, we have isolated and sequenced the complete mouse Bak cDNA...
  17. ncbi Bcl-x and Bax regulate mouse primordial germ cell survival and apoptosis during embryogenesis
    E B Rucker
    Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Mol Endocrinol 14:1038-52. 2000
    ..These findings demonstrate that the balance of Bcl-x and Bax control PGC survival and apoptosis...
  18. pmc tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c
    M C Wei
    Departments of Pathology and Medicine, Harvard Medical School, Dana Farber Cancer Institute, Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA
    Genes Dev 14:2060-71. 2000
    ..b>Bak-deficient mitochondria and blocking antibodies reveal tBID binds to its mitochondrial partner BAK to release ..
  19. ncbi Neuron-specific Bcl-2 homology 3 domain-only splice variant of Bak is anti-apoptotic in neurons, but pro-apoptotic in non-neuronal cells
    Y F Sun
    Program of Molecular Neurobiology, Institute of Biotechnology, University of Helsinki, Viikki Biocenter, FIN 00014 Helsinki, Finland
    J Biol Chem 276:16240-7. 2001
    We have identified and characterized N-Bak, a neuron-specific isoform of the pro-apoptotic Bcl-2 family member Bak...
  20. ncbi Bax and Bak independently promote cytochrome C release from mitochondria
    Kurt Degenhardt
    Department of Molecular Biology, The Cancer Institute of New Jersey, Rutgers University, Piscataway, New Jersey 08854, USA
    J Biol Chem 277:14127-34. 2002
    Pro-apoptotic Bax and Bak have been implicated in the regulation of p53-dependent apoptosis...
  21. ncbi Dynamics of expression of apoptosis-regulatory proteins Bid, Bcl-2, Bcl-X, Bax and Bak during development of murine nervous system
    M Krajewska
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Cell Death Differ 9:145-57. 2002
    ..and immunoblotting to examine the expression of Bid and four other Bcl-2 family proteins (Bcl-2, Bcl-X, Bax and Bak) in the developing and adult murine central nervous system (CNS)...
  22. ncbi Deficiency in Bak and Bax perturbs thymic selection and lymphoid homeostasis
    Jeffrey C Rathmell
    Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Nat Immunol 3:932-9. 2002
    b>Bak and Bax are required and redundant regulators of an intrinsic mitochondrial cell death pathway. To analyze this pathway in T cell development and homeostasis, we reconstituted mice with Bak(-/-)Bax<(-/-) hematopoietic cells...
  23. ncbi Mutational analysis of N-Bak reveals different structural requirements for antiapoptotic activity in neurons and proapoptotic activity in nonneuronal cells
    Yun Fu Sun
    Program in Molecular Neurobiology, Institute of Biotechnology, University of Helsinki, P O Box 56, Viikki Biocenter, Finland
    Mol Cell Neurosci 23:134-43. 2003
    N-Bak, a neuron-specific BH3-only splice variant of Bak, is proapoptotic when overexpressed in nonneuronal cells, but antiapoptotic in NGF-deprived sympathetic neurons...
  24. pmc Nonredundant role of Bax and Bak in Bid-mediated apoptosis
    Pierre Francois Cartron
    INSERM U419, IFR 26, 44035 Nantes Cedex 01 Clinique Universitaire de Neurochirurgie, Hopital G and R Laennec, CHU Nantes, 44093 Nantes Cedex 01, France
    Mol Cell Biol 23:4701-12. 2003
    Animal models suggest that Bax and Bak play an essential role in the implementation of apoptosis and as a result can hinder tumorigenesis. We analyzed the expression of these proteins in 50 human glioblastoma multiforme (GBM) tumors...
  25. ncbi VDAC2 inhibits BAK activation and mitochondrial apoptosis
    Emily H Y Cheng
    Howard Hughes Medical Institute, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Science 301:513-7. 2003
    The multidomain proapoptotic molecules BAK or BAX are required to initiate the mitochondrial pathway of apoptosis...
  26. ncbi The proapoptotic activities of Bax and Bak limit the size of the neural stem cell pool
    Tullia Lindsten
    Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 23:11112-9. 2003
    The proapoptotic Bcl-2 family members Bak and Bax play central and redundant roles in the regulation of apoptosis. In this study, we investigated the effect of loss of Bax and Bak in the CNS...
  27. pmc Constitutive association of the proapoptotic protein Bim with Bcl-2-related proteins on mitochondria in T cells
    Yanan Zhu
    Department of Biochemistry and Molecular Genetics, University of Colorado Health Sciences Center, Denver, CO 80262, USA
    Proc Natl Acad Sci U S A 101:7681-6. 2004
    ..Our results indicate that, in T cells, Bim function is regulated by interaction with Bcl-2 family members on mitochondria rather than by sequestration to the microtubules...
  28. ncbi Hexokinase-mitochondria interaction mediated by Akt is required to inhibit apoptosis in the presence or absence of Bax and Bak
    Nathan Majewski
    Department of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois 60607, USA
    Mol Cell 16:819-30. 2004
    ..of hexokinase from mitochondria potently induce cytochrome c release and apoptosis, even in the absence of Bax and Bak. These effects are inhibited by activated Akt, but not by Bcl-2, implying that changes in outer mitochondrial ..
  29. ncbi Growth factor regulation of autophagy and cell survival in the absence of apoptosis
    Julian J Lum
    Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Cell 120:237-48. 2005
    ..However, using growth factor-dependent cells from Bax/Bak-deficient mice, we demonstrate that apoptosis is not essential to limit cell autonomous survival...
  30. ncbi Bak but not Bax is essential for Bcl-xS-induced apoptosis
    L Lindenboim
    Department of Neurobiochemistry, George S Wise Faculty of Life Sciences, Tel Aviv University, 69978 Ramat Aviv, Tel Aviv, Israel
    Cell Death Differ 12:713-23. 2005
    ..fibroblasts derived from mice deficient in the multidomain proapoptotic members of the Bcl-2 family (Bax and Bak) and the apoptotic components of the apoptosome (Apaf-1 and caspase-9) to unravel the cascade of events by which ..
  31. pmc Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins
    Simon N Willis
    The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia
    Genes Dev 19:1294-305. 2005
    ..proteins trigger apoptosis by binding via their BH3 domain to prosurvival relatives, while the proapoptotic Bax and Bak have an essential downstream role involving permeabilization of organellar membranes and induction of caspase ..
  32. ncbi Specific requirement for Bax, not Bak, in Myc-induced apoptosis and tumor suppression in vivo
    Tobias B Dansen
    Cancer Research Institute and Department of Cellular and Molecular Pharmacology, Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California 94143 0875, USA
    J Biol Chem 281:10890-5. 2006
    Bax and Bak comprise the mitochondrial gateway for apoptosis induced by diverse stimuli...
  33. ncbi Proapoptotic BAX and BAK modulate the unfolded protein response by a direct interaction with IRE1alpha
    Claudio Hetz
    Howard Hughes Medical Institute, Dana Farber Cancer Institute, and Harvard Medical School, Boston, MA 02115, USA
    Science 312:572-6. 2006
    ..We investigated UPR signaling events in mice in the absence of the proapoptotic BCL-2 family members BAX and BAK [double knockout (DKO)]...
  34. ncbi Cell death provoked by loss of interleukin-3 signaling is independent of Bad, Bim, and PI3 kinase, but depends in part on Puma
    Paul G Ekert
    Children s Cancer Centre, Murdoch Children s Research Centre, Royal Children s Hospital, Flemington Rd, Parkville, Victoria 3052, Australia
    Blood 108:1461-8. 2006
    ..IL-3-dependent cell lines from mice lacking the genes for Bad, Bim, Puma, both Bad and Bim, and both Bax and Bak. Surprisingly, Bad was not required for cell death following IL-3 withdrawal, suggesting changes to phosphorylation ..
  35. ncbi The vaccinia virus protein F1L interacts with Bim and inhibits activation of the pro-apoptotic protein Bax
    John M Taylor
    Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
    J Biol Chem 281:39728-39. 2006
    ..We previously showed that F1L interacts with the pro-apoptotic Bcl-2 family member Bak and inhibits activation of Bak following an apoptotic stimulus (Wasilenko, S. T., Banadyga, L., Bond, D...
  36. ncbi Programmed anuclear cell death delimits platelet life span
    Kylie D Mason
    Molecular Genetics of Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia
    Cell 128:1173-86. 2007
    ..Pro-survival Bcl-x(L) constrains the pro-apoptotic activity of Bak to maintain platelet survival, but as Bcl-x(L) degrades, aged platelets are primed for cell death...
  37. pmc Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death
    Christopher P Baines
    Department of Pediatrics, University of Cincinnati, Cincinnati Children s Hospital Medical Center, Cincinnati, OH 45229, USA
    Nat Cell Biol 9:550-5. 2007
    ..These results indicate that Vdacs are dispensable for both MPT and Bcl-2 family member-driven cell death...
  38. pmc Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins
    Craig Brooks
    Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, GA 30912, USA
    Proc Natl Acad Sci U S A 104:11649-54. 2007
    ..Bax and Bak, two multidomain Bcl-2 family proteins, provide a requisite gateway to mitochondrial injury...
  39. ncbi A spatially and temporally restricted mouse model of soft tissue sarcoma
    David G Kirsch
    Center for Cancer Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA
    Nat Med 13:992-7. 2007
    ..Deletion of the Ink4a-Arf locus (Cdkn2a), but not Bak1 and Bax, could substitute for mutation of Trp53 in this model...
  40. pmc Autophagy promotes necrosis in apoptosis-deficient cells in response to ER stress
    E Ullman
    Cell Death Differ 15:422-5. 2008
  41. pmc Caspase-2 cleavage of BID is a critical apoptotic signal downstream of endoplasmic reticulum stress
    John Paul Upton
    Department of Pathology, Medicine, University of California, San Francisco, California 94143, USA
    Mol Cell Biol 28:3943-51. 2008
    ..reticulum (ER) and triggers cell death through activation of the multidomain proapoptotic BCL-2 proteins BAX and BAK at the outer mitochondrial membrane...
  42. doi To trigger apoptosis, Bak exposes its BH3 domain and homodimerizes via BH3:groove interactions
    Grant Dewson
    Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Melbourne, Victoria 3050, Australia
    Mol Cell 30:369-80. 2008
    The Bcl-2 relative Bak is thought to drive apoptosis by forming homo-oligomers that permeabilize mitochondria, but how it is activated and oligomerizes is unclear...
  43. pmc Bcl-XL inhibits membrane permeabilization by competing with Bax
    Lieven P Billen
    Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada
    PLoS Biol 6:e147. 2008
    ..We propose that because Bcl-XL does not oligomerize it functions like a dominant-negative Bax in the membrane permeabilization process...
  44. pmc IL-6 protects against hyperoxia-induced mitochondrial damage via Bcl-2-induced Bak interactions with mitofusins
    Aaron B Waxman
    Pulmonary Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Bulfinch 148, Boston, MA 02114, USA
    Am J Respir Cell Mol Biol 41:385-96. 2009
    ..Finally, Bcl-2 blocked the dissociation of Bak from mitofusin protein (Mfn) 2, and inhibited the interaction between Bak and Mfn1...
  45. doi Two distinct pathways regulate platelet phosphatidylserine exposure and procoagulant function
    Simone M Schoenwaelder
    Australian Centre for Blood Diseases, Monash University, 89 Commercial Road, Melbourne, Victoria 3004, Australia
    Blood 114:663-6. 2009
    ..To clarify this, we investigated the consequence of removing the essential mediators of apoptosis, Bak and Bax, or directly inducing apoptosis with the BH3 mimetic compound ABT-737...
  46. doi Cytomegaloviruses inhibit Bak- and Bax-mediated apoptosis with two separate viral proteins
    M Cam
    Division of Viral Infections, Robert Koch Institute, Nordufer 20, 13353 Berlin, Germany
    Cell Death Differ 17:655-65. 2010
    ..apoptosis by preventing activation and/or oligomerization of the proapoptotic mitochondrial proteins Bax and Bak. Here we show that cytomegaloviruses (CMVs) have adopted a different strategy...
  47. doi Bak activation for apoptosis involves oligomerization of dimers via their alpha6 helices
    Grant Dewson
    The Walter and Eliza Hall Institute of Medical Research, Melbourne, Parkville Victoria, Australia
    Mol Cell 36:696-703. 2009
    A pivotal step toward apoptosis is oligomerization of the Bcl-2 relative Bak. We recently reported that its oligomerization initiates by insertion of an exposed BH3 domain into the groove of another Bak monomer...
  48. pmc Mcl-1 promotes survival of thymocytes by inhibition of Bak in a pathway separate from Bcl-2
    A Dunkle
    Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA
    Cell Death Differ 17:994-1002. 2010
    ..By generation of various genetic mouse models, we found that Mcl-1-deficient thymocytes die largely by a Bak-specific mechanism...
  49. doi Platelet senescence is regulated by an internal timer, not damage inflicted by hits
    Mark R Dowling
    Immunology Division, Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
    Blood 116:1776-8. 2010
    ..Thus, at steady state, platelet senescence is probably the product of internal processes rather than external hits...
  50. pmc Conformational changes in BAK, a pore-forming proapoptotic Bcl-2 family member, upon membrane insertion and direct evidence for the existence of BH3-BH3 contact interface in BAK homo-oligomers
    Kyoung Joon Oh
    Department of Biochemistry, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois 60064, USA
    J Biol Chem 285:28924-37. 2010
    During apoptosis, the pro-apoptotic Bcl-2 family proteins BAK and BAX form large oligomeric pores in the mitochondrial outer membrane...
  51. pmc Bcl-2 family interaction with the mitochondrial morphogenesis machinery
    M M Cleland
    Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
    Cell Death Differ 18:235-47. 2011
    ..Here we report that Bax and Bak participate in the regulation of mitochondrial fusion in mouse embryonic fibroblasts, primary mouse neurons and ..
  52. pmc Blocking the mitochondrial apoptotic pathway preserves motor neuron viability and function in a mouse model of amyotrophic lateral sclerosis
    Nichole A Reyes
    Department of Pathology, University of California, San Francisco, San Francisco, California 94143 0511, USA
    J Clin Invest 120:3673-9. 2010
    ..tissue-specific deletion in the mouse CNS of BCL2-associated X protein (BAX) and BCL2-homologous antagonist/killer (BAK), 2 proapoptotic BCL-2 family proteins that together represent an essential gateway to the mitochondrial apoptotic ..
  53. pmc BH3 domains other than Bim and Bid can directly activate Bax/Bak
    Han Du
    Department of Pathology, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA
    J Biol Chem 286:491-501. 2011
    ..of a subgroup of the Bcl-2 family, known as the BH3-only proteins, activate pro-apoptotic effectors (Bax and Bak) to initiate MOMP. They do so by neutralizing pro-survival Bcl-2 proteins and/or directly activating Bax/Bak...
  54. pmc BH3-only activator proteins Bid and Bim are dispensable for Bak/Bax-dependent thrombocyte apoptosis induced by Bcl-xL deficiency: molecular requisites for the mitochondrial pathway to apoptosis in platelets
    Takahiro Kodama
    Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    J Biol Chem 286:13905-13. 2011
    A pivotal step in the mitochondrial pathway of apoptosis is activation of Bak and Bax, although the molecular mechanism remains controversial...
  55. pmc Transient binding of an activator BH3 domain to the Bak BH3-binding groove initiates Bak oligomerization
    Haiming Dai
    Division of Oncology Research, Department of Oncology, Mayo Clinic, Rochester, MN 55905, USA
    J Cell Biol 194:39-48. 2011
    The mechanism by which the proapoptotic Bcl-2 family members Bax and Bak release cytochrome c from mitochondria is incompletely understood...
  56. pmc Requirement of FADD, NEMO, and BAX/BAK for aberrant mitochondrial function in tumor necrosis factor alpha-induced necrosis
    Krishna M Irrinki
    Department of Biochemistry, Temple University, Philadelphia, PA 19140, USA
    Mol Cell Biol 31:3745-58. 2011
    ..Finally, elimination of BAX and BAK or overexpression of Bcl-x(L) protects cells from necroptosis at a later step...
  57. pmc Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthase
    Kambiz N Alavian
    Department of Internal Medicine, Yale University, New Haven, Connecticut 06520, USA
    Nat Cell Biol 13:1224-33. 2011
    ..Our findings indicate that increased mitochondrial efficiency contributes to the enhanced synaptic efficacy found in Bcl-x(L)-expressing neurons...
  58. pmc A unified model of mammalian BCL-2 protein family interactions at the mitochondria
    Fabien Llambi
    Department of Immunology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Mol Cell 44:517-31. 2011
    ..of exogenous BH3 domains inserted into a tBID backbone that can activate the proapoptotic effectors BAX and BAK to permeabilize membranes without being universally sequestered by all antiapoptotic BCL-2 proteins...
  59. pmc Sphingolipid metabolism cooperates with BAK and BAX to promote the mitochondrial pathway of apoptosis
    Jerry E Chipuk
    Mount Sinai School of Medicine, Department of Oncological Sciences, New York, NY 10029, USA
    Cell 148:988-1000. 2012
    ..We observed that dissociation of heterotypic membranes from mitochondria inhibited BAK/BAX-dependent cytochrome c (cyto c) release...
  60. pmc Bax regulates primary necrosis through mitochondrial dynamics
    Russell S Whelan
    Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 109:6566-71. 2012
    ..Bcl-2 proteins Bax and Bak are the principal activators of MOMP and apoptosis...
  61. pmc Bcl-2, Bcl-x(L), and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells
    Delphine Merino
    The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
    Blood 119:5807-16. 2012
    ..These results have profound implications for how BH3-mimetics induce apoptosis and how the use of these compounds can be optimized for treating lymphoid malignancies...
  62. pmc The BH3-only proteins Bim and Puma cooperate to impose deletional tolerance of organ-specific antigens
    Daniel H D Gray
    Molecular Genetics of Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
    Immunity 37:451-62. 2012
    ..Our data show that Puma cooperates with Bim to impose a thymic-deletion checkpoint to peripheral self-antigens and cement the notion that defects in apoptosis alone are sufficient to cause autoimmune disease...
  63. pmc FOXO3A directs a protective autophagy program in haematopoietic stem cells
    Matthew R Warr
    The Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, Department of Medicine, Division of Hematology Oncology, University of California San Francisco, San Francisco, California 94143, USA
    Nature 494:323-7. 2013
    ..Our results demonstrate that autophagy is essential for the life-long maintenance of the HSC compartment and for supporting an old, failing blood system...
  64. pmc The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues
    T Lindsten
    Department of Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA
    Mol Cell 6:1389-99. 2000
    ..However, mice lacking bax display limited phenotypic abnormalities. As presented here, bak(-/-) mice were found to be developmentally normal and reproductively fit and failed to develop any age-related ..
  65. pmc Essential role of BAX,BAK in B cell homeostasis and prevention of autoimmune disease
    Osamu Takeuchi
    Howard Hughes Medical Institute, Dana Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:11272-7. 2005
    ..Here we show proapoptotic BCL-2 family members BAX and BAK are essential for regulating the number of B cells at both immature and mature developmental stages...
  66. pmc Execution of superoxide-induced cell death by the proapoptotic Bcl-2-related proteins Bid and Bak
    Muniswamy Madesh
    Department of Biochemistry, Temple University, Philadelphia, PA 19140, USA
    Mol Cell Biol 29:3099-112. 2009
    ..and mitochondrial membrane potential loss that is not dependent upon H(2)O(2) and divalent cations and requires Bak in a Bax-independent fashion...
  67. pmc The VDAC2-BAK rheostat controls thymocyte survival
    Decheng Ren
    Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
    Sci Signal 2:ra48. 2009
    The proapoptotic proteins BAX and BAK constitute the mitochondrial apoptotic gateway that executes cellular demise after integrating death signals...
  68. pmc p53 controls radiation-induced gastrointestinal syndrome in mice independent of apoptosis
    David G Kirsch
    David H Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
    Science 327:593-6. 2010
    ..Studying mouse models, we found that selective deletion of the proapoptotic genes Bak1 and Bax from the GI epithelium or from endothelial cells did not protect mice from developing the GI syndrome after ..
  69. pmc BID, BIM, and PUMA are essential for activation of the BAX- and BAK-dependent cell death program
    Decheng Ren
    Molecular Oncology, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
    Science 330:1390-3. 2010
    Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled...
  70. pmc Megakaryocytes possess a functional intrinsic apoptosis pathway that must be restrained to survive and produce platelets
    Emma C Josefsson
    Molecular Medicine Division, Cancer and Hematology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville 3052, Australia Department of Medical Biology, The University of Melbourne, Parkville 3010, Australia
    J Exp Med 208:2017-31. 2011
    ..we generated mice with hematopoietic- or megakaryocyte-specific deletions of the essential mediators of apoptosis, Bak and Bax. We found that platelet production was unperturbed...
  71. pmc Proapoptotic Bak and Bax guard against fatal systemic and organ-specific autoimmune disease
    Kylie D Mason
    The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia
    Proc Natl Acad Sci U S A 110:2599-604. 2013
    ..b>Bak and Bax are two proapoptotic members of the Bcl-2 protein family with overlapping, essential roles in the intrinsic ..
  72. pmc Bok is a pro-apoptotic Bcl-2 protein with restricted expression in reproductive tissues and heterodimerizes with selective anti-apoptotic Bcl-2 family members
    S Y Hsu
    Division of Reproductive Biology, Department of Gynecology and Obstetrics, Stanford University Medical School, Stanford, CA 94305 5317, USA
    Proc Natl Acad Sci U S A 94:12401-6. 1997
    ..This finding is in direct contrast to the ability of other pro-apoptotic members (Bax, Bak, and Bik) to interact with all of the anti-apoptotic proteins...
  73. ncbi Neurons exclusively express N-Bak, a BH3 domain-only Bak isoform that promotes neuronal apoptosis
    Takuma Uo
    Department of Neurological Surgery, University of Washington School of Medicine, Box 356470, Seattle, Washington 98195 6470, USA
    J Biol Chem 280:9065-73. 2005
    b>Bak is generally recognized as a multidomain, pro-apoptotic member of the Bcl-2 family. Bak and Bax are functionally redundant in non-neuronal cells and represent a mitochondrial convergence point for cell death signaling pathways...
  74. pmc Loss of Bif-1 suppresses Bax/Bak conformational change and mitochondrial apoptosis
    Yoshinori Takahashi
    Drug Discovery Program, H Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, Tampa, FL 33612, USA
    Mol Cell Biol 25:9369-82. 2005
    ..Here, we provide evidence that Bif-1 plays a regulatory role in apoptotic activation of not only Bax but also Bak and appears to be involved in suppression of tumorigenesis...
  75. pmc BI-1 regulates endoplasmic reticulum Ca2+ homeostasis downstream of Bcl-2 family proteins
    Chunyan Xu
    Program on Apoptosis and Cell Death Research, Burnham Institute for Medical Research, La Jolla, California 92037, USA
    J Biol Chem 283:11477-84. 2008
    ..In bax(-/-)bak(-/-) double knock-out cells, both BI-1 and Bcl-X(L) retained their ability to reduce [Ca(2+)](er), suggesting that ..
  76. ncbi Induction of apoptosis by the Bcl-2 homologue Bak
    T Chittenden
    Apoptosis Technology Inc, Cambridge, Massachusetts 02139, USA
    Nature 374:733-6. 1995
    ..Here we describe the complementary DNA cloning and functional analysis of a new Bcl-2 homologue, Bak, which promotes cell death and counteracts the protection from apoptosis provided by Bcl-2...
  77. ncbi c-Myc sensitization to oxygen deprivation-induced cell death is dependent on Bax/Bak, but is independent of p53 and hypoxia-inducible factor-1
    Joslyn K Brunelle
    Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611 3010, USA
    J Biol Chem 279:4305-12. 2004
    ..Our results demonstrate that murine embryonic fibroblasts from bax-/-bak-/- mice that conditionally express c-Myc did not die in response to either oxygen or serum deprivation...
  78. pmc Bnip3 impairs mitochondrial bioenergetics and stimulates mitochondrial turnover
    S Rikka
    Department of Pharmacology, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA 92093 0758, USA
    Cell Death Differ 18:721-31. 2011
    ..between mitochondrial dysfunction and upregulation of autophagy in response to Bnip3 in cells lacking Bax and Bak. We found that Bnip3 induced mitochondrial autophagy in the absence of mitochondrial membrane permeabilization and ..
  79. doi Bak deficiency inhibits liver carcinogenesis: a causal link between apoptosis and carcinogenesis
    Hayato Hikita
    Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    J Hepatol 57:92-100. 2012
    ....
  80. ncbi Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K
    S N Farrow
    Molecular Science Department, Glaxo Research and Development Ltd, Greenford, Middlesex, UK
    Nature 374:731-3. 1995
    ..One of these is a new member of the bcl-2 family, which we have called bak (for bcl-2 homologous antagonist/killer)...
  81. pmc Expression of Bcl-2 family during liver regeneration and identification of Bcl-x as a delayed early response gene
    S P Tzung
    Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104, USA
    Am J Pathol 150:1985-95. 1997
    ..The three pro-apoptotic members of the family, Bak, Bad, and Bax, all showed an early decline in mRNA levels when Bcl-x transcripts increased, followed by later peaks ..
  82. ncbi Developmental expression patterns of Bcl-2, Bcl-x, Bax, and Bak in teeth
    S Krajewski
    The Burnham Institute formerly La Jolla Cancer Research Foundation, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Cell Death Differ 5:408-15. 1998
    The ontogenic profile of expression of four members of the Bcl-2 family (Bcl-2, Bcl-x, Bax and Bak) was examined in the mouse by immunohistochemistry using paraffin sections...
  83. pmc Epistatic and independent functions of caspase-3 and Bcl-X(L) in developmental programmed cell death
    K A Roth
    Department of Pathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 97:466-71. 2000
    ....
  84. ncbi Pro- and anti-apoptotic members of the Bcl-2 family in skeletal muscle: a distinct role for Bcl-2 in later stages of myogenesis
    J A Dominov
    Myogenesis Research Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    Dev Dyn 220:18-26. 2001
    ..Both anti-apoptotic (Bcl-W, Bcl-X(L)) and pro-apoptotic (Bad, Bak, Bax) members of the Bcl-2 family were expressed in developing skeletal muscle in vivo...
  85. ncbi Essential roles of the Bcl-2 family of proteins in caspase-2-induced apoptosis
    Zhonghua Gao
    Cell Biology Program, Memorial Sloan Kettering Cancer Center, Cornell University Weill Graduate School of Medical Sciences, New York, New York 10021, USA
    J Biol Chem 280:38271-5. 2005
    ..Caspase-2 was not able to induce cytochrome c release from Bax(-/-)Bak(-/-) mitochondria either...
  86. pmc Concomitant loss of proapoptotic BH3-only Bcl-2 antagonists Bik and Bim arrests spermatogenesis
    Leigh Coultas
    The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
    EMBO J 24:3963-73. 2005
    ..Thus, Bik and Bim share, upstream of Bax, the role of eliminating supernumerary germ cells during the first wave of spermatogenesis, a process vital for normal testicular development...
  87. ncbi Constitutive androstane receptor (CAR) ligand, TCPOBOP, attenuates Fas-induced murine liver injury by altering Bcl-2 proteins
    Edwina S Baskin-Bey
    Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Hepatology 44:252-62. 2006
    ..The proapoptotic proteins Bak (Bcl-2 antagonistic killer) and Bax (Bcl-2-associated X protein) were depleted in livers from TCPOBOP-treated CAR+/+..
  88. ncbi Crosstalk between Bak/Bax and mTOR signaling regulates radiation-induced autophagy
    Luigi Moretti
    Department of Radiation Oncology, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 5671, USA
    Autophagy 3:142-4. 2007
    Bax and Bak, act as a gateway for caspase-mediated cell death. mTOR, an Akt downstream effector, plays a critical role in cell proliferation, growth and survival...
  89. pmc Hepatic IGFBP1 is a prosurvival factor that binds to BAK, protects the liver from apoptosis, and antagonizes the proapoptotic actions of p53 at mitochondria
    J I Ju Leu
    Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    Genes Dev 21:3095-109. 2007
    ..a portion of intracellular IGFBP1 protein localizes to mitochondria where it binds to the proapoptotic protein BAK and hinders BAK activation and apoptosis induction...
  90. doi Hax1-mediated processing of HtrA2 by Parl allows survival of lymphocytes and neurons
    Jyh Rong Chao
    Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Nature 452:98-102. 2008
    ..Together, the results identify a previously unknown sequence of interactions involving a Bcl-2-family-related protein and mitochondrial proteases in the ability to resist the induction of apoptosis when cytokines are limiting...
  91. pmc Apoptosis and autophagy induction in mammalian cells by small interfering RNA knockdown of mRNA capping enzymes
    Chun Chu
    Center for Advanced Biotechnology and Medicine, 679 Hoes Lane, Piscataway, NJ 08854, USA
    Mol Cell Biol 28:5829-36. 2008
    ..Induction of apoptosis was independent of p53 tumor suppressor but dependent on BAK or BAX...
  92. doi Triggering of apoptosis by Puma is determined by the threshold set by prosurvival Bcl-2 family proteins
    Bernard A Callus
    Department of Biochemistry, La Trobe University, Victoria 3086, Australia
    J Mol Biol 384:313-23. 2008
    ..Puma co-immunoprecipitated endogenous Bcl-2 and Mcl-1 but not Bax and Bak, suggesting that Puma did not associate with either Bax or Bak in these cells to initiate cell death...
  93. pmc Mechanism of apoptosis induction by inhibition of the anti-apoptotic BCL-2 proteins
    Jerry E Chipuk
    Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Proc Natl Acad Sci U S A 105:20327-32. 2008
    ..permeabilization (MOMP) by regulating the activation of the pro-apoptotic BCL-2 effector molecules, BAX and BAK. Sustainable cellular stress induces proteins (e.g...
  94. pmc The Isopeptidase Inhibitor G5 Triggers a Caspase-independent Necrotic Death in Cells Resistant to Apoptosis: A COMPARATIVE STUDY WITH THE PROTEASOME INHIBITOR BORTEZOMIB
    Alessandra Fontanini
    Dipartimento di Scienze e Tecnologie Biomediche, Sezione di Biologia, and MATI Center of Excellence
    J Biol Chem 284:8369-81. 2009
    ..apoptosis-proficient wild type mouse embryo fibroblasts and on cells defective for apoptosis (double-deficient Bax/Bak mouse embryo fibroblasts) (double knockout; DKO)...
  95. pmc Assembly of the mitochondrial apoptosis-induced channel, MAC
    Sonia Martinez-Caballero
    Department of Basic Sciences, New York University College of Dentistry, New York, New York 10010, USA
    J Biol Chem 284:12235-45. 2009
    ..clamp studies of mitochondria isolated from cells deficient in one or both of the pro-apoptotic proteins Bax and Bak show that at least one of the proteins must be present for formation of the cytochrome c-translocating channel, ..
  96. doi Granulysin induces cathepsin B release from lysosomes of target tumor cells to attack mitochondria through processing of bid leading to Necroptosis
    Honglian Zhang
    National Laboratory of Biomacromolecules and Center for Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China
    J Immunol 182:6993-7000. 2009
    ..Cathepsin B silencing and Bid or Bax/Bak deficiency resists granulysin-induced cytochrome c and apoptosis-activating factor release and is less susceptible ..
  97. pmc Ars2 links the nuclear cap-binding complex to RNA interference and cell proliferation
    Joshua J Gruber
    Abramson Family Cancer Research Institute and Department of Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Cell 138:328-39. 2009
    ..These findings provide evidence for a role for Ars2 in RNA interference regulation during cell proliferation...
  98. pmc Maintenance of the relative proportion of oligodendrocytes to axons even in the absence of BAX and BAK
    Kumi Kawai
    Department of Neurology, University of California, School of Medicine, Sacramento, CA, USA
    Eur J Neurosci 30:2030-41. 2009
    Highly purified oligodendroglial lineage cells from mice lacking functional bax and bak genes were resistant to apoptosis after in-vitro differentiation, indicating an essential role of the intrinsic apoptotic pathway in apoptosis of ..
  99. pmc The BCL-2 protein BAK is required for long-chain ceramide generation during apoptosis
    Leah J Siskind
    Ralph H Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401, USA
    J Biol Chem 285:11818-26. 2010
    The BCL-2 family members BAK and BAX are required for apoptosis and trigger mitochondrial outer membrane permeabilization (MOMP)...
  100. pmc Single-point mutations of a lysine residue change function of Bax and Bcl-xL expressed in Bax- and Bak-less mouse embryonic fibroblasts: novel insights into the molecular mechanisms of Bax-induced apoptosis
    I Szabo
    Department of Biology, University of Padova, Padova, Italy
    Cell Death Differ 18:427-38. 2011
    ..This substitution turned Bcl-x(L) proapoptotic. Transfection of double knockout (Bax(-/-)/Bak(-/-)) mouse embryonic fibroblasts (DKO MEFs) with either wild-type Bax, BaxK128E, or Bcl-x(L)E158K showed that ..
  101. doi Sensitivity to antitubulin chemotherapeutics is regulated by MCL1 and FBW7
    Ingrid E Wertz
    Department of Early Discovery Biochemistry, Genentech, South San Francisco, California 94080, USA
    Nature 471:110-4. 2011
    ..Our findings suggest that profiling the FBW7 and MCL1 status of tumours, in terms of protein levels, messenger RNA levels and genetic status, could be useful to predict the response of patients to antitubulin chemotherapeutics...

Research Grants3

  1. Metabolomics: From Bioenergetics To Apoptosis
    Craig Thompson; Fiscal Year: 2005
    ..Understanding the relationships between metabolism and apoptosis may lead to novel approaches for the prevention and/or treatment of cancer and degenerative disorders. ..
  2. Il-6 type cytokine protection from hyperoxic lung injury
    Aaron Waxman; Fiscal Year: 2007
    ..abstract_text> ..
  3. Lymphocyte Survival: Implications for lymphomagenesis
    Craig B Thompson; Fiscal Year: 2010
    ....