M Kawabata

Summary

Affiliation: University of Tokyo
Country: Japan

Publications

  1. ncbi Signal transduction of the TGF-beta superfamily by Smad proteins
    M Kawabata
    Department of Biochemistry, The Cancer Institute, Japanese Foundation for Cancer Research JFCR, Toshima ku, Tokyo 170 8455, Japan
    J Biochem 125:9-16. 1999
  2. ncbi Intracellular signaling of the TGF-beta superfamily by Smad proteins
    M Kawabata
    Department of Biochemistry, Cancer Institute, Japanese Foundation for Cancer Research JFCR, Tokyo, Japan
    Ann N Y Acad Sci 886:73-82. 1999
  3. ncbi Signal transduction by bone morphogenetic proteins
    M Kawabata
    Department of Biochemistry, The Cancer Institute, Tokyo, Japan
    Cytokine Growth Factor Rev 9:49-61. 1998
  4. ncbi Interplay of signal mediators of decapentaplegic (Dpp): molecular characterization of mothers against dpp, Medea, and daughters against dpp
    H Inoue
    Department of Biochemistry, The Cancer Institute, Japanese Foundation for Cancer Research, and Research for the Future Program, Japan Society for the Promotion of Science, Tokyo 170 8455, Japan
    Mol Biol Cell 9:2145-56. 1998
  5. ncbi Roles of bone morphogenetic protein type I receptors and Smad proteins in osteoblast and chondroblast differentiation
    M Fujii
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research and Research for the Future Program, Tokyo, Japan
    Mol Biol Cell 10:3801-13. 1999
  6. ncbi Schnurri interacts with Mad in a Dpp-dependent manner
    Y Udagawa
    Department of Biochemistry, The Cancer Institute of Japanese Foundation for Cancer Research JFCR, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    Genes Cells 5:359-69. 2000
  7. ncbi Interaction and functional cooperation of PEBP2/CBF with Smads. Synergistic induction of the immunoglobulin germline Calpha promoter
    J Hanai
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 70 8455, Japan
    J Biol Chem 274:31577-82. 1999
  8. ncbi c-Ski acts as a transcriptional co-repressor in transforming growth factor-beta signaling through interaction with smads
    S Akiyoshi
    Department of Biochemistry, The Cancer Institute of Japanese Foundation for Cancer Research, Research for the Future Program, Japan Society for Promotion of Science, 1 37 1, Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    J Biol Chem 274:35269-77. 1999
  9. ncbi Alpha-helix 2 in the amino-terminal mad homology 1 domain is responsible for specific DNA binding of Smad3
    K Kusanagi
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170-8455, Japan
    J Biol Chem 276:28155-63. 2001
  10. ncbi Ligand-dependent degradation of Smad3 by a ubiquitin ligase complex of ROC1 and associated proteins
    M Fukuchi
    Department of Biochemistry, The Cancer Institute of Japanese Foundation for Cancer Research, and Research for the Future Program, the Japan Society for the Promotion of Science, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    Mol Biol Cell 12:1431-43. 2001

Collaborators

Detail Information

Publications21

  1. ncbi Signal transduction of the TGF-beta superfamily by Smad proteins
    M Kawabata
    Department of Biochemistry, The Cancer Institute, Japanese Foundation for Cancer Research JFCR, Toshima ku, Tokyo 170 8455, Japan
    J Biochem 125:9-16. 1999
    ..R-Smads interact with transcriptional coactivators, and have intrinsic transactivation activity. Elucidation of the functions of Smads will provide the framework for research on TGF-beta superfamily signaling...
  2. ncbi Intracellular signaling of the TGF-beta superfamily by Smad proteins
    M Kawabata
    Department of Biochemistry, Cancer Institute, Japanese Foundation for Cancer Research JFCR, Tokyo, Japan
    Ann N Y Acad Sci 886:73-82. 1999
    ..Thus, the missense mutation not only disrupts the function of the wild-type Smad but also creates a dominant-negative Smad, which could actively contribute to oncogenesis...
  3. ncbi Signal transduction by bone morphogenetic proteins
    M Kawabata
    Department of Biochemistry, The Cancer Institute, Tokyo, Japan
    Cytokine Growth Factor Rev 9:49-61. 1998
    ..In Drosophila melanogaster, Decapentaplegic (Dpp) is a homologue of mammalian BMPs. In this review, mechanism of action of Dpp will be discussed in comparison with that of BMPs...
  4. ncbi Interplay of signal mediators of decapentaplegic (Dpp): molecular characterization of mothers against dpp, Medea, and daughters against dpp
    H Inoue
    Department of Biochemistry, The Cancer Institute, Japanese Foundation for Cancer Research, and Research for the Future Program, Japan Society for the Promotion of Science, Tokyo 170 8455, Japan
    Mol Biol Cell 9:2145-56. 1998
    ..We also show that Mad exists as a monomer in the absence of Tkv stimulation. Tkv induces homo-oligomerization of Mad, and Dad inhibits this step. Finally, we propose a model for Dpp signaling by Drosophila Smad proteins...
  5. ncbi Roles of bone morphogenetic protein type I receptors and Smad proteins in osteoblast and chondroblast differentiation
    M Fujii
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research and Research for the Future Program, Tokyo, Japan
    Mol Biol Cell 10:3801-13. 1999
    ..Osteoblast differentiation induced by BMPs is thus mediated mainly via the Smad-signaling pathway, whereas chondrogenic differentiation may be transmitted by Smad-dependent and independent pathways...
  6. ncbi Schnurri interacts with Mad in a Dpp-dependent manner
    Y Udagawa
    Department of Biochemistry, The Cancer Institute of Japanese Foundation for Cancer Research JFCR, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    Genes Cells 5:359-69. 2000
    ..schnurri (shn) was identified as a candidate gene acting downstream of Dpp receptors, but its relevance to Mad has remained unknown...
  7. ncbi Interaction and functional cooperation of PEBP2/CBF with Smads. Synergistic induction of the immunoglobulin germline Calpha promoter
    J Hanai
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 70 8455, Japan
    J Biol Chem 274:31577-82. 1999
    ..PEBP2 may thus be a nuclear target of TGF-beta/BMP signaling...
  8. ncbi c-Ski acts as a transcriptional co-repressor in transforming growth factor-beta signaling through interaction with smads
    S Akiyoshi
    Department of Biochemistry, The Cancer Institute of Japanese Foundation for Cancer Research, Research for the Future Program, Japan Society for Promotion of Science, 1 37 1, Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    J Biol Chem 274:35269-77. 1999
    ..c-Ski is thus a transcriptional co-repressor that links Smads to HDAC in TGF-beta signaling...
  9. ncbi Alpha-helix 2 in the amino-terminal mad homology 1 domain is responsible for specific DNA binding of Smad3
    K Kusanagi
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170-8455, Japan
    J Biol Chem 276:28155-63. 2001
    ..Smad3 thus binds to DNA directly through the beta-hairpin loop, and H2 supports specific DNA binding of Smad3...
  10. ncbi Ligand-dependent degradation of Smad3 by a ubiquitin ligase complex of ROC1 and associated proteins
    M Fukuchi
    Department of Biochemistry, The Cancer Institute of Japanese Foundation for Cancer Research, and Research for the Future Program, the Japan Society for the Promotion of Science, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    Mol Biol Cell 12:1431-43. 2001
    ..Smad3 bound to ROC1-SCF(Fbw1a) is then exported from the nucleus to the cytoplasm for proteasomal degradation. TGF-beta/Smad3 signaling is thus irreversibly terminated by the ubiquitin-proteasome pathway...
  11. ncbi Interaction of Drosophila inhibitors of apoptosis with thick veins, a type I serine/threonine kinase receptor for decapentaplegic
    E Oeda
    Department of Biochemistry, The Cancer Institute, Tokyo, Japanese Foundation for Cancer Research and Research for the Future Program, Japan Society for the Promotion of Science, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    J Biol Chem 273:9353-6. 1998
    ..These data suggest that DIAP1 and DIAP2 may be involved, possibly as negative regulators, in the Dpp signaling pathway, which leads to cell apoptosis...
  12. ncbi Smad6 inhibits signalling by the TGF-beta superfamily
    T Imamura
    Department of Biochemistry, The Cancer Institute, Tokyo, Japan
    Nature 389:622-6. 1997
    ..These data indicate that signals of the TGF-beta superfamily are regulated both positively and negatively by members of the SMAD family...
  13. ncbi E1A inhibits transforming growth factor-beta signaling through binding to Smad proteins
    A Nishihara
    Department of Biochemistry, The Cancer Institute of Japanese Foundation for Cancer Research, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    J Biol Chem 274:28716-23. 1999
    ..We found that E1A interacts specifically with receptor-regulated Smads, suggesting a novel mechanism whereby E1A antagonizes TGF-beta signaling...
  14. ncbi Targets of transcriptional regulation by transforming growth factor-beta: expression profile analysis using oligonucleotide arrays
    S Akiyoshi
    Department of Biochemistry, The Cancer Institute of Japanese Foundation for Cancer Research (JFCR, and Research for the Future Program, the Japan Society for the Promotion of Science, Toshima-ku, Tokyo 170-8455, Japan
    Jpn J Cancer Res 92:257-68. 2001
    ..Taken together, the results suggest that TGF-beta may suppress tumorigenesis through positive and negative regulation of transcription...
  15. ncbi Characterization of bone morphogenetic protein-6 signaling pathways in osteoblast differentiation
    T Ebisawa
    Department of Biochemistry, The Cancer Institute of JFCR, and Research for the Future Program, Japan Society for the Promotion of Science, Toshima ku, Tokyo 170 8455, Japan
    J Cell Sci 112:3519-27. 1999
    ..These findings indicate that in the process of differentiation to osteoblasts, BMP-6 binds to ALK-2 as well as other type I receptors, and transduces signals mainly through Smad5 and possibly through Smad1...
  16. ncbi Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1
    M Saitoh
    Department of Biochemistry, The Cancer Institute, Tokyo, Japanese Foundation for Cancer Research, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 170, Japan
    EMBO J 17:2596-606. 1998
    ..The evidence that Trx is a negative regulator of ASK1 suggests possible mechanisms for redox regulation of the apoptosis signal transduction pathway as well as the effects of antioxidants against cytokine- and stress-induced apoptosis...
  17. ncbi BMP type II receptor is required for gastrulation and early development of mouse embryos
    H Beppu
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, Research for the Future Program, Japan Society for the Promotion of Science, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo, 170 8455, Japan
    Dev Biol 221:249-58. 2000
    ..Our results suggest that the function of BMPR-II is essential for epiblast differentiation and mesoderm induction during early mouse development...
  18. ncbi Synergistic signaling in fetal brain by STAT3-Smad1 complex bridged by p300
    K Nakashima
    Department of Molecular Cell Biology, Cell Fate Modulation Research Unit, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 101 0062, Japan
    Science 284:479-82. 1999
    ..The formation of a complex between STAT3 and Smad1, bridged by p300, is involved in the cooperative signaling of LIF and BMP2 and the subsequent induction of astrocytes from neural progenitors...
  19. ncbi Drosophila dSmad2 and Atr-I transmit activin/TGFbeta signals
    P Das
    Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854 8020, USA
    Genes Cells 4:123-34. 1999
    ....
  20. ncbi Smads, TAK1, and their common target ATF-2 play a critical role in cardiomyocyte differentiation
    K Monzen
    Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan
    J Cell Biol 153:687-98. 2001
    ..These results suggest that Smads, TAK1, and their common target ATF-2 cooperatively play a critical role in cardiomyocyte differentiation...
  21. ncbi Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators
    J Yanagisawa
    Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Bunkyo ku, Tokyo 113 0032, Japan
    Science 283:1317-21. 1999
    ..Thus, Smad3 may mediate cross-talk between vitamin D and TGF-beta signaling pathways...