Kohei Miyazono

Summary

Affiliation: University of Tokyo
Country: Japan

Publications

  1. ncbi Negative regulation of transforming growth factor-beta (TGF-beta) signaling by WW domain-containing protein 1 (WWP1)
    Akiyoshi Komuro
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Oncogene 23:6914-23. 2004
  2. ncbi Id: a target of BMP signaling
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Sci STKE 2002:pe40. 2002
  3. ncbi Signal transduction by bone morphogenetic protein receptors: functional roles of Smad proteins
    K Miyazono
    Department of Biochemistry, The Cancer Institute, Japanese Foundation for Cancer Research, Japan Society for the Promotion of Science, Tokyo
    Bone 25:91-3. 1999
  4. ncbi Positive and negative regulation of TGF-beta signaling
    K Miyazono
    Department of Biochemistry, the Cancer Institute of the 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
    J Cell Sci 113:1101-9. 2000
  5. ncbi TGF-beta signaling by Smad proteins
    K Miyazono
    Department of Biochemistry, the Cancer Institute of the Japanese Foundation for Cancer Research JFCR, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo, Japan
    Cytokine Growth Factor Rev 11:15-22. 2000
  6. ncbi Ninth Japanese-German Workshop on Molecular and Cellular Aspects of Carcinogenesis, Essen, Germany, 18-20 September, 2003
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Cancer Sci 95:276-81. 2004
  7. ncbi TGF-beta/SMAD signaling and its involvement in tumor progression
    K Miyazono
    Department of Biochemistry, The Center Institute of the Japanese Foundation for Cancer Research, Tokyo, Japan
    Biol Pharm Bull 23:1125-30. 2000
  8. ncbi Divergence and convergence of TGF-beta/BMP signaling
    K Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo ku, Tokyo Japan
    J Cell Physiol 187:265-76. 2001
  9. ncbi Regulation of transforming growth factor-beta signaling and vascular diseases
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Cancer Institute of the Japanese Foundation for Cancer Research, Japan
    Cornea 21:S48-53. 2002
  10. ncbi Tenth Japanese-German Workshop on Molecular and Cellular Aspects of Carcinogenesis, Essen, Germany, 29 September-1 October 2005
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. [corrected
    Cancer Sci 97:332-9. 2006

Detail Information

Publications152 found, 100 shown here

  1. ncbi Negative regulation of transforming growth factor-beta (TGF-beta) signaling by WW domain-containing protein 1 (WWP1)
    Akiyoshi Komuro
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Oncogene 23:6914-23. 2004
    ..Importantly, WWP1 and Smurfs were expressed in distinct patterns in human tissues and carcinoma cell lines, suggesting unique pathophysiological roles of WWP1 and Smurfs...
  2. ncbi Id: a target of BMP signaling
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Sci STKE 2002:pe40. 2002
    ..Growing evidence suggests that Id proteins may play crucial roles in angiogenesis, neurogenesis, and osteogenesis and act as key molecules in regulating biological responses induced by BMPs and TGF-beta...
  3. ncbi Signal transduction by bone morphogenetic protein receptors: functional roles of Smad proteins
    K Miyazono
    Department of Biochemistry, The Cancer Institute, Japanese Foundation for Cancer Research, Japan Society for the Promotion of Science, Tokyo
    Bone 25:91-3. 1999
    ..Anti-Smads are induced by ligand stimulation, suggesting that they constitute a negative feedback loop in the signal transduction pathways of the TGF-beta superfamily...
  4. ncbi Positive and negative regulation of TGF-beta signaling
    K Miyazono
    Department of Biochemistry, the Cancer Institute of the 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
    J Cell Sci 113:1101-9. 2000
    ..Regulation of TGF-beta signaling might be tightly linked to tumor progression, since TGF-beta is a potent growth inhibitor in most cell types...
  5. ncbi TGF-beta signaling by Smad proteins
    K Miyazono
    Department of Biochemistry, the Cancer Institute of the Japanese Foundation for Cancer Research JFCR, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo, Japan
    Cytokine Growth Factor Rev 11:15-22. 2000
    ..Through interaction with different transcription factors and transcriptional co-activators or co-repressors, Smads may exhibit specific effects in various cell types...
  6. ncbi Ninth Japanese-German Workshop on Molecular and Cellular Aspects of Carcinogenesis, Essen, Germany, 18-20 September, 2003
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Cancer Sci 95:276-81. 2004
    ..Additional support from many other sponsors in Germany and Japan is gratefully acknowledged. The Workshop participants are listed at the end of this Report...
  7. ncbi TGF-beta/SMAD signaling and its involvement in tumor progression
    K Miyazono
    Department of Biochemistry, The Center Institute of the Japanese Foundation for Cancer Research, Tokyo, Japan
    Biol Pharm Bull 23:1125-30. 2000
    ..Perturbation of the TGF-beta/SMAD signaling pathway may result in progression of tumors through resistance of the cells to the growth inhibition induced by TGF-beta...
  8. ncbi Divergence and convergence of TGF-beta/BMP signaling
    K Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo ku, Tokyo Japan
    J Cell Physiol 187:265-76. 2001
    ..Perturbations of the TGF-beta/BMP signaling pathways result in various clinical disorders including cancers, vascular diseases, and bone disorders...
  9. ncbi Regulation of transforming growth factor-beta signaling and vascular diseases
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Cancer Institute of the Japanese Foundation for Cancer Research, Japan
    Cornea 21:S48-53. 2002
    ....
  10. ncbi Tenth Japanese-German Workshop on Molecular and Cellular Aspects of Carcinogenesis, Essen, Germany, 29 September-1 October 2005
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. [corrected
    Cancer Sci 97:332-9. 2006
  11. ncbi Regulation of TGF-beta signaling and its roles in progression of tumors
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Japan
    Cancer Sci 94:230-4. 2003
    ..Abnormalities of these regulators of TGF-beta signaling may thus participate in the progression of various tumors...
  12. ncbi BMP receptor signaling: transcriptional targets, regulation of signals, and signaling cross-talk
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Cytokine Growth Factor Rev 16:251-63. 2005
    ..Moreover, recent findings have revealed that BMP pathways interact with other signaling pathways, and such signaling cross-talk plays pivotal roles in growth and differentiation of target cells...
  13. ncbi NEDD4-2 (neural precursor cell expressed, developmentally down-regulated 4-2) negatively regulates TGF-beta (transforming growth factor-beta) signalling by inducing ubiquitin-mediated degradation of Smad2 and TGF-beta type I receptor
    Go Kuratomi
    Department of Biochemistry, the Cancer Institute of the Japanese Foundation for Cancer Research JFCR, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    Biochem J 386:461-70. 2005
    ....
  14. ncbi Interaction with Smad4 is indispensable for suppression of BMP signaling by c-Ski
    Masafumi Takeda
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Japan
    Mol Biol Cell 15:963-72. 2004
    ..We also found that c-Ski interacted with Smad3 or Smad4 without disrupting Smad3-Smad4 heteromer formation. c-Ski (ARPG) would be useful for selectively suppressing TGF-beta/activin signaling...
  15. ncbi Diffuse-type gastric carcinoma: progression, angiogenesis, and transforming growth factor beta signaling
    Akiyoshi Komuro
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Hongo 7 3 1, Bunkyo ku, Tokyo, Japan
    J Natl Cancer Inst 101:592-604. 2009
    ..However, the association of TGF-beta signaling with diffuse-type gastric carcinoma has not been investigated in detail...
  16. ncbi c-Ski overexpression promotes tumor growth and angiogenesis through inhibition of transforming growth factor-beta signaling in diffuse-type gastric carcinoma
    Kunihiko Kiyono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    Cancer Sci 100:1809-16. 2009
    ..These findings suggest that c-Ski overexpression promotes the growth of diffuse-type gastric carcinoma through induction of angiogenesis...
  17. ncbi Arkadia amplifies TGF-beta superfamily signalling through degradation of Smad7
    Daizo Koinuma
    Department of Biochemistry, the Cancer Institute of the Japanese Foundation for Cancer Research JFCR, Toshima ku, Tokyo, Japan
    EMBO J 22:6458-70. 2003
    ..Arkadia may thus play an important role as an amplifier of TGF-beta superfamily signalling under both physiological and pathological conditions...
  18. ncbi Arkadia induces degradation of SnoN and c-Ski to enhance transforming growth factor-beta signaling
    Yoshiko Nagano
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Bunkyo ku, Tokyo 113 0033, Japan
    J Biol Chem 282:20492-501. 2007
    ....
  19. ncbi Cooperative inhibition of bone morphogenetic protein signaling by Smurf1 and inhibitory Smads
    Gyo Murakami
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, Tokyo 170 8455, Japan
    Mol Biol Cell 14:2809-17. 2003
    ..Moreover, Smurf1 associated with Smad1/5 indirectly through I-Smads and induced their ubiquitination and degradation. Smurf1 thus controls BMP signaling with and without I-Smads through multiple mechanisms...
  20. ncbi Nuclear and cytoplasmic c-Ski differently modulate cellular functions
    Motoko Nagata
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113 0033, Japan
    Genes Cells 11:1267-80. 2006
    ..Mapping of the regions required for cytoplasmic accumulation by proteasome inhibitors suggests that subcellular localization of c-Ski may be regulated by proteasome-sensitive processes through amino acid residues 94-210 and 491-548...
  21. ncbi Two short segments of Smad3 are important for specific interaction of Smad3 with c-Ski and SnoN
    Masafumi Mizuide
    Department of Biochemistry, the Cancer Institute of the Japanese Foundation for Cancer Research JFCR, Tokyo 170 8455, Japan
    J Biol Chem 278:531-6. 2003
    ..Our findings thus demonstrate the stoichiometry of how multiple molecules can associate with the Smad oligomers and how the Smad-interacting proteins functionally interact with each other...
  22. ncbi Regulation of transforming growth factor-beta and bone morphogenetic protein signalling by transcriptional coactivator GCN5
    Kaoru Kahata
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, 1 37 1 Kami Ikebukuro, Toshima ku, Tokyo 170 8455, Japan
    Genes Cells 9:143-51. 2004
    ..In conclusion we identified GCN5 as a Smad-binding transcriptional coactivator which positively regulates both TGF-beta and BMP signalling pathways...
  23. ncbi BMP-9 induces proliferation of multiple types of endothelial cells in vitro and in vivo
    Yuka Suzuki
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113 0033, Japan
    J Cell Sci 123:1684-92. 2010
    ..These findings suggest that BMP-9 signaling activates the endothelium tested in the present study via ALK-1...
  24. ncbi SKI and MEL1 cooperate to inhibit transforming growth factor-beta signal in gastric cancer cells
    Mami Takahata
    Division of Biochemistry, the Cancer Institute of the Japanese Foundation for Cancer Research JFCR, Division of Molecular Pharmacology, the Cancer Chemotherapy Center of the JFCR, and Genome Center of the JFCR, Tokyo, Japan
    J Biol Chem 284:3334-44. 2009
    ..These findings reveal a novel mechanism where distinct transcriptional co-repressors are co-amplified and functionally interact, and provide molecular targets for gastric cancer treatment...
  25. ncbi Exogenous introduction of tissue inhibitor of metalloproteinase 2 reduces accelerated growth of TGF-β-disrupted diffuse-type gastric carcinoma
    Erik Johansson
    Department of Molecular Pathology and the Global Center of Excellence Program for Integrative Life Science Based on the Study of Biosignaling Mechanisms, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    Cancer Sci 101:2398-403. 2010
    ..These findings provide evidence that one of the mechanisms of the increase in angiogenesis in diffuse-type gastric carcinoma is the downregulation of the anti-angiogenic protein TIMP2...
  26. ncbi Smad7 inhibits transforming growth factor-beta family type i receptors through two distinct modes of interaction
    Yuto Kamiya
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Bunkyo ku, Tokyo 113 0033, Japan
    J Biol Chem 285:30804-13. 2010
    ..Smad7 thus has an additional mode of interaction with TGF-β family type I receptors not possessed by Smad6, which may play roles in mediating the inhibitory effects unique to Smad7...
  27. ncbi Pin1 down-regulates transforming growth factor-beta (TGF-beta) signaling by inducing degradation of Smad proteins
    Ayako Nakano
    Division of Biochemistry, the Cancer Institute of the Japanese Foundation for Cancer Research JFCR, Tokyo 135 8550, Japan
    J Biol Chem 284:6109-15. 2009
    ..Pin1 inhibited TGF-beta-induced transcription and gene expression, suggesting that Pin1 negatively regulates TGF-beta signaling by down-regulating Smad2/3 protein levels via induction of Smurf2-mediated ubiquitin-proteasomal degradation...
  28. ncbi Antiangiogenic gene therapy of experimental pancreatic tumor by sFlt-1 plasmid DNA carried by RGD-modified crosslinked polyplex micelles
    Yelena Vachutinsky
    Department of Bioengineering, Graduate School of Engineering, The University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 8656, Japan
    J Control Release 149:51-7. 2011
    ..These results suggest that RGD targeted crosslinked polyplex micelles can be effective plasmid DNA carriers for antiangiogenic gene therapy...
  29. ncbi Comparison of the effects of the kinase inhibitors imatinib, sorafenib, and transforming growth factor-beta receptor inhibitor on extravasation of nanoparticles from neovasculature
    Mitsunobu R Kano
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo, 113 0033, Japan
    Cancer Sci 100:173-80. 2009
    ..In conclusion, the appropriate strategy for optimization of tumor vasculature for nanoparticles may differ depending on tumor type, and in particular on the degree of pericyte coverage around the vasculature...
  30. ncbi Roles for the MH2 domain of Smad7 in the specific inhibition of transforming growth factor-beta superfamily signaling
    Toshiaki Mochizuki
    Department of Biochemistry, Cancer Institute of the Japanese Foundation for Cancer Research JFCR, Tokyo 170 8455, Japan
    J Biol Chem 279:31568-74. 2004
    ..Thus, the MH2 domain of Smad7 plays important roles in specific inhibition of TGF-beta superfamily signals through differential interaction with type I receptors...
  31. ncbi Identification of targets of Prox1 during in vitro vascular differentiation from embryonic stem cells: functional roles of HoxD8 in lymphangiogenesis
    Kaori Harada
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113 0033, Japan
    J Cell Sci 122:3923-30. 2009
    ..These findings indicate that transcriptional networks of Prox1 and HoxD8 play important roles in the maturation and maintenance of lymphatic vessels...
  32. ncbi An Id-like molecule, HHM, is a synexpression group-restricted regulator of TGF-beta signalling
    Hiroaki Ikushima
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    EMBO J 27:2955-65. 2008
    ..HHM thus appears to regulate a subset of TGF-beta target genes including the Olig1-Smad synexpression group. HHM is the first example of a cellular response-selective regulator of TGF-beta signalling with clearly determined mechanisms...
  33. ncbi Antiangiogenic gene therapy of solid tumor by systemic injection of polyplex micelles loading plasmid DNA encoding soluble flt-1
    Makoto Oba
    Department of Clinical Vascular Regeneration, Graduate School of Medicine, The University of Tokyo, 7 3 1 Hongo, Bunkyo, Tokyo 113 8655, Japan
    Mol Pharm 7:501-9. 2010
    ..Therefore, the disulfide cross-linked polyplex micelle loading sFlt-1 pDNA has a great potential for antiangiogenic therapy against subcutaneous pancreatic tumor model by systemic application...
  34. ncbi Context-dependent regulation of the expression of c-Ski protein by Arkadia in human cancer cells
    Yoshiko Nagano
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Hongo 7 3 1, Bunkyo ku, Tokyo, Japan
    J Biochem 147:545-54. 2010
    ..Arkadia thus regulates the levels of expression of c-Ski protein in cell-type-dependent fashion, and exhibits a tumour suppressor function by inhibiting tumour cell growth...
  35. ncbi Functional heterogeneity of bone morphogenetic protein receptor-II mutants found in patients with primary pulmonary hypertension
    Ayako Nishihara
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Japan
    Mol Biol Cell 13:3055-63. 2002
    ..The differences in biological activities among the BMPR-II mutants observed thus suggest that additional genetic and/or environmental factors may play critical roles in the pathogenesis of PPH...
  36. ncbi TGF-β regulates isoform switching of FGF receptors and epithelial-mesenchymal transition
    Takuya Shirakihara
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    EMBO J 30:783-95. 2011
    ..Thus, TGF-β and FGF-2 may cooperate with each other and may regulate EMT of various kinds of cells in cancer microenvironment during cancer progression...
  37. ncbi Autophagy is activated by TGF-beta and potentiates TGF-beta-mediated growth inhibition in human hepatocellular carcinoma cells
    Kunihiko Kiyono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    Cancer Res 69:8844-52. 2009
    ..These findings show that TGF-beta signaling pathway activates autophagy in certain human cancer cells and that induction of autophagy is a novel aspect of biological functions of TGF-beta...
  38. ncbi c-Ski activates MyoD in the nucleus of myoblastic cells through suppression of histone deacetylases
    Norihiko Kobayashi
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Genes Cells 12:375-85. 2007
    ..We conclude that c-Ski induces myogenic differentiation through acting on MyoD and inhibiting HDAC activity in the nucleus of myogenic cells...
  39. ncbi Inhibition of endogenous TGF-beta signaling enhances lymphangiogenesis
    Masako Oka
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    Blood 111:4571-9. 2008
    ..These findings suggest that TGF-beta transduces signals in LECs and plays an important role in the regulation of lymphangiogenesis in vivo...
  40. ncbi Transforming growth factor-beta promotes survival of mammary carcinoma cells through induction of antiapoptotic transcription factor DEC1
    Shogo Ehata
    Department of Biochemistry, Cancer Institute of the Japanese Foundation for Cancer Research, Tokyo, Japan
    Cancer Res 67:9694-703. 2007
    ..Our observations thus provide new insights into the molecular mechanisms governing TGF-beta-mediated cell survival and metastasis of cancer...
  41. ncbi c-Ski inhibits the TGF-beta signaling pathway through stabilization of inactive Smad complexes on Smad-binding elements
    Hiroyuki Suzuki
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113 0033, Japan
    Oncogene 23:5068-76. 2004
    ..These results suggest that stabilization of inactive Smad complexes on DNA is a critical event in c-Ski-mediated inhibition of TGF-beta signaling...
  42. ncbi Tob proteins enhance inhibitory Smad-receptor interactions to repress BMP signaling
    Yutaka Yoshida
    Department of Oncology, The Institute of Medical Science, University of Tokyo, 4 6 1 Shirokanedai, Minato ku, Tokyo 108, Japan
    Mech Dev 120:629-37. 2003
    ..Our results provide both in vitro and in vivo evidence that Tob inhibits endogenous BMP signaling by facilitating inhibitory Smad functions...
  43. ncbi Thyroid transcription factor-1 inhibits transforming growth factor-beta-mediated epithelial-to-mesenchymal transition in lung adenocarcinoma cells
    Roy Akira Saito
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Bunkyo ku, Tokyo, Japan
    Cancer Res 69:2783-91. 2009
    ....
  44. ncbi Cell type-specific target selection by combinatorial binding of Smad2/3 proteins and hepatocyte nuclear factor 4alpha in HepG2 cells
    Anna Mizutani
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    J Biol Chem 286:29848-60. 2011
    ....
  45. ncbi Arkadia complexes with clathrin adaptor AP2 and regulates EGF signalling
    Anna Mizutani
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo, Japan
    J Biochem 148:733-41. 2010
    ..Arkadia thus appears to regulate EGF signalling by modulating endocytosis of EGFR through interaction with AP2 complex...
  46. ncbi Endogenous TGF-beta signaling suppresses maturation of osteoblastic mesenchymal cells
    Shingo Maeda
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, Tokyo
    EMBO J 23:552-63. 2004
    ....
  47. ncbi TGF-beta signaling in embryonic stem cell-derived endothelial cells
    Tetsuro Watabe
    Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Japan
    Methods Mol Biol 330:341-51. 2006
    ..In this chapter, we present how to study the cellular and biochemical effects of TGF-beta signals on endothelial cells derived from mouse ESCs...
  48. ncbi BMP signals inhibit proliferation and in vivo tumor growth of androgen-insensitive prostate carcinoma cells
    Hideyo Miyazaki
    Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Oncogene 23:9326-35. 2004
    ..Furthermore, this is the first report of a role for BMP signaling in reducing growth kinetics of androgen-insensitive prostate tumors...
  49. ncbi Pitx2 prevents osteoblastic transdifferentiation of myoblasts by bone morphogenetic proteins
    Makoto Hayashi
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, 3 10 6 Ariake, Koto ku, Tokyo 135 8550, Japan
    J Biol Chem 283:565-71. 2008
    ..These findings suggest that Pitx2 suppresses osteogenic signals induced by BMPs in myoblasts to prevent their osteoblastic conversion...
  50. ncbi Transforming growth factor-beta signaling is differentially inhibited by Smad2D450E and Smad3D407E
    Miki Kondo
    Department of Biochemistry, the Cancer Institute of the Japanese Foundation for Cancer Research JFCR, Toshima ku, Tokyo 170 8455, Japan
    Cancer Sci 95:12-7. 2004
    ....
  51. ncbi Negative regulation of BMP/Smad signaling by Tob in osteoblasts
    Y Yoshida
    Department of Oncology, The Institute of Medical Science, University of Tokyo, Minato ku, Tokyo 108 8639, Japan
    Cell 103:1085-97. 2000
    ..The results indicate that Tob negatively regulates osteoblast proliferation and differentiation by suppressing the activity of the receptor-regulated Smad proteins...
  52. ncbi SB-431542 and Gleevec inhibit transforming growth factor-beta-induced proliferation of human osteosarcoma cells
    Shigeo Matsuyama
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Cancer Res 63:7791-8. 2003
    ....
  53. ncbi miR-135b mediates NPM-ALK-driven oncogenicity and renders IL-17-producing immunophenotype to anaplastic large cell lymphoma
    Hironori Matsuyama
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Japan
    Blood 118:6881-92. 2011
    ..These results collectively illuminated unique contribution of oncogenic kinase-linked microRNA to tumorigenesis through modulation of tumor immune-phenotype and microenvironment...
  54. ncbi Homozygously deleted gene DACH1 regulates tumor-initiating activity of glioma cells
    Akira Watanabe
    Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan
    Proc Natl Acad Sci U S A 108:12384-9. 2011
    ..These results illustrate that DACH1 is a distinctive tumor suppressor, which does not only suppress growth of tumor cells but also regulates bFGF-mediated tumor-initiating activity of glioma cells...
  55. ncbi VEGFR2-PLCgamma1 axis is essential for endothelial specification of VEGFR2+ vascular progenitor cells
    Hitoshi Sase
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Hongo, Tokyo, Japan
    J Cell Sci 122:3303-11. 2009
    ..Taken together, these findings indicate that VEGFR2-PLCgamma1 signal relay gives rise to the unique function of VEGFR2, thus enabling endothelial differentiation from vascular progenitors...
  56. ncbi Ets family members induce lymphangiogenesis through physical and functional interaction with Prox1
    Yasuhiro Yoshimatsu
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113 0033, Japan
    J Cell Sci 124:2753-62. 2011
    ..Furthermore, we found that both Prox1 and Ets-2 bind to the VEGFR3 promoter in intact chromatin. These findings suggest that Ets family members function as transcriptional cofactors that enhance Prox1-induced lymphangiogenesis...
  57. ncbi Receptor tyrosine kinases inhibit bone morphogenetic protein-Smad responsive promoter activity and differentiation of murine MC3T3-E1 osteoblast-like cells
    Konosuke Nakayama
    Division of Endocrinology, Department of Medicine, University of Tokyo School of Medicine, Tokyo, Japan
    J Bone Miner Res 18:827-35. 2003
    ..Because direct phosphorylation of Smad1 by ERKs is not required for the inhibition, other transcriptional factors that are phosphorylated by ERKs might be involved in the regulation of osteoblastic differentiation by ERKs...
  58. ncbi Chromatin immunoprecipitation on microarray analysis of Smad2/3 binding sites reveals roles of ETS1 and TFAP2A in transforming growth factor beta signaling
    Daizo Koinuma
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, Koto ku, Tokyo 135 8550, Japan
    Mol Cell Biol 29:172-86. 2009
    ..These findings reveal novel regulatory mechanisms of Smad2/3-induced transcription and provide an essential resource for understanding their roles...
  59. ncbi Polyplex micelles from triblock copolymers composed of tandemly aligned segments with biocompatible, endosomal escaping, and DNA-condensing functions for systemic gene delivery to pancreatic tumor tissue
    Kanjiro Miyata
    Department of Bioengineering, Graduate School of Engineering, The University of Tokyo, Tokyo, Japan
    Pharm Res 25:2924-36. 2008
    ....
  60. ncbi TGF-beta receptor kinase inhibitor enhances growth and integrity of embryonic stem cell-derived endothelial cells
    Tetsuro Watabe
    Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan
    J Cell Biol 163:1303-11. 2003
    ..These results suggest that endogenous TGF-beta/activin signals play important roles in regulating vascular growth and permeability...
  61. ncbi Enhanced magnetic resonance imaging of experimental pancreatic tumor in vivo by block copolymer-coated magnetite nanoparticles with TGF-beta inhibitor
    Michiaki Kumagai
    Department of Materials Engineering, Graduate School of Engineering, The University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 8656, Japan
    J Control Release 140:306-11. 2009
    ..Use of the PEG-PAsp-coated magnetite nanoparticles, combined with the TGF-beta inhibitor, is of promising clinical importance for the detection of intractable solid cancers, including pancreatic cancer...
  62. ncbi Smad4-independent regulation of p21/WAF1 by transforming growth factor-beta
    Hideaki Ijichi
    Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 8655, Japan
    Oncogene 23:1043-51. 2004
    ..The upregulation occurs through Smad2/3-dependent transcriptional activation of the p21/WAF1 promoter region. These results suggest a novel mechanism of gene regulation, that is, a novel signal mediator other than Smad4...
  63. ncbi Improvement of cancer-targeting therapy, using nanocarriers for intractable solid tumors by inhibition of TGF-beta signaling
    Mitsunobu R Kano
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113 0033 Japan
    Proc Natl Acad Sci U S A 104:3460-5. 2007
    ..The use of TbetaR-I inhibitor combined with nanocarriers may thus be of significant clinical and practical importance in treating intractable solid cancers...
  64. ncbi Lymphoid enhancer factor 1 makes cells resistant to transforming growth factor beta-induced repression of c-myc
    Toru Sasaki
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, Tokyo 170-8455, Japan
    Cancer Res 63:801-6. 2003
    ..These findings suggest that enhanced expression of LEF-1, which occurs frequently in colon cancer, may make cells refractory to the down-regulation of c-myc and the subsequent growth arrest induced by TGF-beta...
  65. ncbi Chromosomal region maintenance 1 (CRM1)-dependent nuclear export of Smad ubiquitin regulatory factor 1 (Smurf1) is essential for negative regulation of transforming growth factor-beta signaling by Smad7
    Yoshitaka Tajima
    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 278:10716-21. 2003
    ..These results thus suggest that CRM1-dependent nuclear export of Smurf1 is essential for the negative regulation of TGF-beta signaling by Smad7...
  66. ncbi Smurf1 regulates the inhibitory activity of Smad7 by targeting Smad7 to the plasma membrane
    Chie Suzuki
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    J Biol Chem 277:39919-25. 2002
    ..Thus, these results suggest that the plasma membrane localization of Smad7 by Smurf1 requires the C2 domain of Smurf1 and is essential for the inhibitory effect of Smad7 in the transforming growth factor-beta signaling pathway...
  67. ncbi Snail is required for TGFbeta-induced endothelial-mesenchymal transition of embryonic stem cell-derived endothelial cells
    Takashi Kokudo
    Department of Molecular Pathology, Graduate School of Medicine and the Global Center of Excellence Program for Integrative Life Science Based on the Study of Biosignaling Mechanisms, The University of Tokyo, Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    J Cell Sci 121:3317-24. 2008
    ..These results indicate that Snail mediates the actions of endogenous TGFbeta signals that induce EndMT...
  68. ncbi Role of Ras signaling in the induction of snail by transforming growth factor-beta
    Kana Horiguchi
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Tokyo 113 0033, Japan
    J Biol Chem 284:245-53. 2009
    ....
  69. ncbi Ras signaling directs endothelial specification of VEGFR2+ vascular progenitor cells
    Kyoko Kawasaki
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Bunkyo, Tokyo 113 0033, Japan
    J Cell Biol 181:131-41. 2008
    ..VEGF-A thus activates temporally distinct Ras-Erk signaling to direct endothelial specification of VEGFR2(+) vascular progenitor cells...
  70. 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...
  71. ncbi CCAAT/enhancer-binding protein homologous protein (CHOP) regulates osteoblast differentiation
    Ken Shirakawa
    Department of Biochemistry, the Cancer Institute of the Japanese Foundation for Cancer Research JFCR, 3 10 6, Ariake, Koto ku, Tokyo 135 8550, Japan
    Mol Cell Biol 26:6105-16. 2006
    ..Thus, endogenous CHOP may have dual roles in regulating osteoblast differentiation and bone formation...
  72. ncbi A crucial role of a high mobility group protein HMGA2 in cardiogenesis
    Koshiro Monzen
    Department of Cardiovascular Medicine, The University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 8655, Japan
    Nat Cell Biol 10:567-74. 2008
    ..5 gene, both in P19CL6 cells and in transgenic Xenopus embryos. Thus, HMGA2 is a positive regulator of Nkx2.5 gene expression and is essential for normal cardiac development...
  73. 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...
  74. ncbi Stimulation of Smad1 transcriptional activity by Ras-extracellular signal-regulated kinase pathway: a possible mechanism for collagen-dependent osteoblastic differentiation
    Miyuki Suzawa
    Institute of Molecular and Cellular Biosciences, University of Tokyo, Japan
    J Bone Miner Res 17:240-8. 2002
    ....
  75. ncbi Smurf1 interacts with transforming growth factor-beta type I receptor through Smad7 and induces receptor degradation
    T Ebisawa
    Department of Biochemistry, The Cancer Institute of the 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
    J Biol Chem 276:12477-80. 2001
    ..These results thus reveal a novel function of Smad7, i.e. induction of degradation of TbetaR-I through recruitment of an E3 ligase to the receptor...
  76. ncbi Axin facilitates Smad3 activation in the transforming growth factor beta signaling pathway
    M Furuhashi
    Department of Biochemistry, The Japanese Foundation for Cancer Research JFCR Cancer Institute, Toshima ku, Tokyo 170 8455, Japan
    Mol Cell Biol 21:5132-41. 2001
    ..Axin may thus function as an adapter of Smad3, facilitating its activation by TGF-beta receptors for efficient TGF-beta signaling...
  77. 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...
  78. 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...
  79. ncbi Synergistic effects of different bone morphogenetic protein type I receptors on alkaline phosphatase induction
    H Aoki
    Dept of Biochemistry, The JFCR Cancer Institute, and Research for the Future Program, the Japan Society for the Promotion of Science, Toshima ku, Tokyo 170 8455, Japan
    J Cell Sci 114:1483-9. 2001
    ..Thus, ALK-2 and ALK-3 (or ALK-6) might synergistically induce osteoblast differentiation of C2C12 cells, possibly through efficient activation of downstream signaling pathways...
  80. ncbi Differential regulation of epithelial and mesenchymal markers by deltaEF1 proteins in epithelial mesenchymal transition induced by TGF-beta
    Takuya Shirakihara
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Mol Biol Cell 18:3533-44. 2007
    ....
  81. 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...
  82. 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...
  83. 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...
  84. 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...
  85. ncbi Transforming growth factor-beta signaling in epithelial-mesenchymal transition and progression of cancer
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    Proc Jpn Acad Ser B Phys Biol Sci 85:314-23. 2009
    ..The discovery of molecules that inhibit TGF-beta-induced EMT but not TGF-beta-induced growth arrest may be an ideal strategy for treatment of invasion and metastasis of cancer...
  86. ncbi Roles of TGF-beta family signaling in stem cell renewal and differentiation
    Tetsuro Watabe
    Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Cell Res 19:103-15. 2009
    ..Here, we illustrate the roles of TGF-beta family members in the maintenance and differentiation of ES cells, somatic stem cells, and cancer stem cells...
  87. ncbi Regulation of the stability of cell surface E-cadherin by the proteasome
    Masao Saitoh
    Department of Molecular Pathology, University of Tokyo, Bunkyo ku, Japan
    Biochem Biophys Res Commun 381:560-5. 2009
    ..However, promotion of cell migration by TGF-beta was not significantly affected by proteasome inhibition. Proteasome-dependent events thus appear to be involved in stabilization of cell surface E-cadherin...
  88. ncbi Vasorin, a transforming growth factor beta-binding protein expressed in vascular smooth muscle cells, modulates the arterial response to injury in vivo
    Yuichi Ikeda
    Division of Hematopoietic Factors and Department of Advanced Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108 8639, Japan
    Proc Natl Acad Sci U S A 101:10732-7. 2004
    ..Thus, vasorin is a potential therapeutic target for vascular fibroproliferative disorders...
  89. ncbi Coordinate regulation of cell growth and differentiation by TGF-beta superfamily and Runx proteins
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7 3 1 Hongo, Bunkyo ku, Tokyo 113 0033, Japan
    Oncogene 23:4232-7. 2004
    ....
  90. ncbi A new partner for inhibitory Smads
    Kohei Miyazono
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, 113-0033, Tokyo, Japan
    Cytokine Growth Factor Rev 13:7-9. 2002
  91. ncbi Transforming growth factor-beta up-regulates CD40-engaged IL-12 production of mouse Langerhans cells
    Y Tada
    Department of Dermatology, University of Tokyo, Tokyo, Japan
    Eur J Immunol 31:294-300. 2001
    ....
  92. ncbi A role for Id in the regulation of TGF-beta-induced epithelial-mesenchymal transdifferentiation
    M Kondo
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
    Cell Death Differ 11:1092-101. 2004
    ....
  93. ncbi The N domain of Smad7 is essential for specific inhibition of transforming growth factor-beta signaling
    A Hanyu
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, Tokyo 170-8455, Japan
    J Cell Biol 155:1017-27. 2001
    ..The N domain of Smad7 thus plays an important role in the specific inhibition of TGF-beta signaling...
  94. 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...
  95. ncbi Two major Smad pathways in TGF-beta superfamily signalling
    Keiji Miyazawa
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Japan
    Genes Cells 7:1191-204. 2002
    ..Understanding the mechanisms of TGF-beta superfamily signalling is thus important for the development of new ways to treat various clinical diseases in which TGF-beta superfamily signalling is involved...
  96. ncbi Expression of osterix inhibits bone morphogenetic protein-induced chondrogenic differentiation of mesenchymal progenitor cells
    Hiroyuki Tominaga
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, 3 10 6 Ariake, Koto ku, Tokyo 135 8550, Japan
    J Bone Miner Metab 27:36-45. 2009
    ..These results suggest that the low levels of osterix expression remaining after knockdown are sufficient to block chondrogenesis, whereas higher expression may be required to promote osteoblastic differentiation...
  97. ncbi c-myc is a downstream target of the Smad pathway
    Ken Yagi
    Department of Biochemistry, The Cancer Institute of the 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 277:854-61. 2002
    ..TGF-beta signaling did not compete with E2F-4 for binding to TIE/E2F, but reduced p300 co-immunoprecipitating with E2F-4. Therefore, TGF-beta signaling may suppress c-myc promoter activity by dissociating p300 from E2F-4...
  98. ncbi Targets of transcriptional regulation by two distinct type I receptors for transforming growth factor-beta in human umbilical vein endothelial cells
    Tatsuru Ota
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    J Cell Physiol 193:299-318. 2002
    ..These results revealed some new targets of TGF-beta in endothelial cells, and differences in transcriptional regulation patterns between ALK-1 and ALK-5...
  99. ncbi TGFbeta signalling: a complex web in cancer progression
    Hiroaki Ikushima
    Department of Molecular Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113 0033, Japan
    Nat Rev Cancer 10:415-24. 2010
    ....
  100. ncbi Functional domains of Runx1 are differentially required for CD4 repression, TCRbeta expression, and CD4/8 double-negative to CD4/8 double-positive transition in thymocyte development
    Masahito Kawazu
    Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    J Immunol 174:3526-33. 2005
    ..These results suggest that the activation domain is essential for Runx1 to establish thymocyte development and that Runx1 has both TLE-dependent and TLE-independent functions in thymocyte development...
  101. ncbi The ALK-5 inhibitor A-83-01 inhibits Smad signaling and epithelial-to-mesenchymal transition by transforming growth factor-beta
    Masayoshi Tojo
    Department of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research (JFCR, Ariake, Koto-ku, Tokyo
    Cancer Sci 96:791-800. 2005
    ..Consistent with these findings, A-83-01 inhibited the epithelial-to-mesenchymal transition induced by TGF-beta, suggesting that A-83-01 and related molecules may be useful for preventing the progression of advanced cancers...