Toshiyuki Araki

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Shp2 regulates SRC family kinase activity and Ras/Erk activation by controlling Csk recruitment
    Si Qing Zhang
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115 USA
    Mol Cell 13:341-55. 2004
  2. ncbi request reprint Mouse model of Noonan syndrome reveals cell type- and gene dosage-dependent effects of Ptpn11 mutation
    Toshiyuki Araki
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, NRB1038, 330 Brookline Ave, Boston, Massachusetts 02215, USA
    Nat Med 10:849-57. 2004
  3. ncbi request reprint Tyrosyl phosphorylation of Shp2 is required for normal ERK activation in response to some, but not all, growth factors
    Toshiyuki Araki
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    J Biol Chem 278:41677-84. 2003
  4. ncbi request reprint An Shp2/SFK/Ras/Erk signaling pathway controls trophoblast stem cell survival
    Wentian Yang
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
    Dev Cell 10:317-27. 2006
  5. pmc Receptor-specific regulation of phosphatidylinositol 3'-kinase activation by the protein tyrosine phosphatase Shp2
    Si Qing Zhang
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 22:4062-72. 2002
  6. pmc Activation of multiple signaling pathways causes developmental defects in mice with a Noonan syndrome–associated Sos1 mutation
    Peng Chieh Chen
    Department of Genetics, Harvard Medical School, Boston, Massachusetts, USA
    J Clin Invest 120:4353-65. 2010
  7. pmc Noonan syndrome cardiac defects are caused by PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation
    Toshiyuki Araki
    Division of Hematology Oncology and Cancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 106:4736-41. 2009
  8. pmc A germline gain-of-function mutation in Ptpn11 (Shp-2) phosphatase induces myeloproliferative disease by aberrant activation of hematopoietic stem cells
    Dan Xu
    Department of Medicine, Division of Hematology Oncology, Center for Stem Cell and Regenerative Medicine, Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH 44106, USA
    Blood 116:3611-21. 2010
  9. pmc Control of CNS cell-fate decisions by SHP-2 and its dysregulation in Noonan syndrome
    Andrée S Gauthier
    Developmental Biology Program, Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada
    Neuron 54:245-62. 2007
  10. ncbi request reprint Germline gain-of-function mutations in SOS1 cause Noonan syndrome
    Amy E Roberts
    Harvard Partners Center for Genetics and Genomics and Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Genet 39:70-4. 2007

Collaborators

Detail Information

Publications17

  1. ncbi request reprint Shp2 regulates SRC family kinase activity and Ras/Erk activation by controlling Csk recruitment
    Si Qing Zhang
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115 USA
    Mol Cell 13:341-55. 2004
    ..Decreased phosphorylation/activation of other SFK substrates may explain additional consequences of Shp2 deficiency, including altered cell spreading, stress fibers, focal adhesions, and motility...
  2. ncbi request reprint Mouse model of Noonan syndrome reveals cell type- and gene dosage-dependent effects of Ptpn11 mutation
    Toshiyuki Araki
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, NRB1038, 330 Brookline Ave, Boston, Massachusetts 02215, USA
    Nat Med 10:849-57. 2004
    ....
  3. ncbi request reprint Tyrosyl phosphorylation of Shp2 is required for normal ERK activation in response to some, but not all, growth factors
    Toshiyuki Araki
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    J Biol Chem 278:41677-84. 2003
    ....
  4. ncbi request reprint An Shp2/SFK/Ras/Erk signaling pathway controls trophoblast stem cell survival
    Wentian Yang
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
    Dev Cell 10:317-27. 2006
    ..Bim depletion substantially blocks apoptosis and significantly restores Shp2 null TS cell proliferation, thereby establishing a key mechanism by which FGF4 controls stem cell survival...
  5. pmc Receptor-specific regulation of phosphatidylinositol 3'-kinase activation by the protein tyrosine phosphatase Shp2
    Si Qing Zhang
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 22:4062-72. 2002
    ..Activation of PI3K-dependent pathways following stimulation by other growth factors is unaffected or decreased in Shp2 mutant cells. Thus, Shp2 regulates the kinetics and magnitude of RTK signaling in a receptor-specific manner...
  6. pmc Activation of multiple signaling pathways causes developmental defects in mice with a Noonan syndrome–associated Sos1 mutation
    Peng Chieh Chen
    Department of Genetics, Harvard Medical School, Boston, Massachusetts, USA
    J Clin Invest 120:4353-65. 2010
    ....
  7. pmc Noonan syndrome cardiac defects are caused by PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation
    Toshiyuki Araki
    Division of Hematology Oncology and Cancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 106:4736-41. 2009
    ..Our data provide a mechanistic underpinning for the cardiac defects in this disorder...
  8. pmc A germline gain-of-function mutation in Ptpn11 (Shp-2) phosphatase induces myeloproliferative disease by aberrant activation of hematopoietic stem cells
    Dan Xu
    Department of Medicine, Division of Hematology Oncology, Center for Stem Cell and Regenerative Medicine, Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH 44106, USA
    Blood 116:3611-21. 2010
    ..Collectively, our data suggest that oncogenic Ptpn11 induces MPD by aberrant activation of HSCs. This study also identifies Gab2 as an important mediator for the pathogenic effects of Ptpn11 mutations...
  9. pmc Control of CNS cell-fate decisions by SHP-2 and its dysregulation in Noonan syndrome
    Andrée S Gauthier
    Developmental Biology Program, Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada
    Neuron 54:245-62. 2007
    ....
  10. ncbi request reprint Germline gain-of-function mutations in SOS1 cause Noonan syndrome
    Amy E Roberts
    Harvard Partners Center for Genetics and Genomics and Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Genet 39:70-4. 2007
    ..Our results identify SOS1 mutants as a major cause of Noonan syndrome, representing the first example of activating GEF mutations associated with human disease and providing new insights into RAS-GEF regulation...
  11. ncbi request reprint Shp-2 positively regulates brain-derived neurotrophic factor-promoted survival of cultured ventral mesencephalic dopaminergic neurons through a brain immunoglobulin-like molecule with tyrosine-based activation motifs/Shp substrate-1
    Satomi Takai
    Division of Protein Biosynthesis, Institute for Protein Research, Osaka University, Suita, Japan
    J Neurochem 82:353-64. 2002
    ..Dephosphorylation of BIT/SHPS-1 by Shp-2 may participate in BDNF-stimulated survival signaling...
  12. ncbi request reprint Macrocyclization in the design of non-phosphorus-containing Grb2 SH2 domain-binding ligands
    Zhen Dan Shi
    Laboratory of Medicinal Chemistry, CCR, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, USA
    J Med Chem 47:2166-9. 2004
    ..In extracellular assays affinity was enhanced approximately 5-fold relative to an open-chain congener. Enhancement was also observed in whole-cell assays examining blockade of Grb2 binding to the erbB-2 protein-tyrosine kinase...
  13. ncbi request reprint Artemin is a vascular-derived neurotropic factor for developing sympathetic neurons
    Yutaka Honma
    Department of Pathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neuron 35:267-82. 2002
    ..The chemoattractive properties of ARTN were confirmed by the demonstration that sympathetic neuroblasts migrate and project axons toward ARTN-soaked beads implanted into mouse embryos...
  14. ncbi request reprint Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration
    Toshiyuki Araki
    Department of Pathology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Science 305:1010-3. 2004
    ..These findings suggest that novel therapeutic strategies directed at increasing the supply of NAD and/or Sir2 activation may be effective for treatment of diseases characterized by axonopathy and neurodegeneration...
  15. ncbi request reprint Expression of CD47/integrin-associated protein induces death of cultured cerebral cortical neurons
    Hisatsugu Koshimizu
    Division of Protein Biosynthesis, Institute for Protein Research, Osaka University, Suita, Japan
    J Neurochem 82:249-57. 2002
    ..CD47/IAP-induced death of cultured cortical neurons may be regulated by the interaction of CD47/IAP with BIT/SHPS-1 and by BDNF...
  16. ncbi request reprint Nab proteins are essential for peripheral nervous system myelination
    Nam Le
    Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, Box 8118, Saint Louis, Missouri 63110, USA
    Nat Neurosci 8:932-40. 2005
    ....
  17. ncbi request reprint Nerve growth factor-induced glutamate release is via p75 receptor, ceramide, and Ca(2+) from ryanodine receptor in developing cerebellar neurons
    Tadahiro Numakawa
    Neuronics R G Special Division for Human Life Technology National Institute of Advanced Industrial Science and Technology AIST Midorigaoka, Ikeda, Osaka 563 8577, Japan
    J Biol Chem 278:41259-69. 2003
    ..Thus, we demonstrate that NGF-mediated neurotransmitter release via the p75-dependent pathway has an important role in developing neurons...