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Vol. 10, Issue 11, 3801-3813, November 1999



and
*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, Tokyo 170-8455, Japan;
The biological effects of type I serine/threonine kinase receptors
and Smad proteins were examined using an adenovirus-based vector
system. Constitutively active forms of bone morphogenetic protein (BMP)
type I receptors (BMPR-IA and BMPR-IB; BMPR-I group) and those of
activin receptor-like kinase (ALK)-1 and ALK-2 (ALK-1 group) induced
alkaline phosphatase activity in C2C12 cells. Receptor-regulated Smads (R-Smads) that act in the BMP pathways, such as Smad1 and Smad5,
also induced the alkaline phosphatase activity in C2C12 cells. BMP-6
dramatically enhanced alkaline phosphatase activity induced by Smad1 or
Smad5, probably because of the nuclear translocation of R-Smads
triggered by the ligand. Inhibitory Smads, i.e., Smad6 and Smad7,
repressed the alkaline phosphatase activity induced by BMP-6 or the
type I receptors. Chondrogenic differentiation of ATDC5 cells
was induced by the receptors of the BMPR-I group but not by those of
the ALK-1 group. However, kinase-inactive forms of the receptors of the
ALK-1 and BMPR-I groups blocked chondrogenic differentiation. Although
R-Smads failed to induce cartilage nodule formation, inhibitory Smads
blocked it. 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.
Department of Biomaterials Science and
Second Department of Oral Surgery, Faculty of Dentistry,
Tokyo Medical and Dental University, Tokyo 113-8549, Japan; and
§Creative BioMolecules, Hopkinton, Massachusetts 01748
Corresponding author. E-mail address:
fjios2{at}dent.tmd.ac.jp.
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P. Tylzanowski, K. Verschueren, D. Huylebroeck, and F. P. Luyten Smad-interacting Protein 1 Is a Repressor of Liver/Bone/Kidney Alkaline Phosphatase Transcription in Bone Morphogenetic Protein-induced Osteogenic Differentiation of C2C12 Cells J. Biol. Chem., October 19, 2001; 276(43): 40001 - 40007. [Abstract] [Full Text] [PDF] |
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H Aoki, M Fujii, T Imamura, K Yagi, K Takehara, M Kato, and K Miyazono Synergistic effects of different bone morphogenetic protein type I receptors on alkaline phosphatase induction J. Cell Sci., January 4, 2001; 114(8): 1483 - 1489. [Abstract] [PDF] |
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F. De Luca, K. M. Barnes, J. A. Uyeda, S. De-Levi, V. Abad, T. Palese, V. Mericq, and J. Baron Regulation of Growth Plate Chondrogenesis by Bone Morphogenetic Protein-2 Endocrinology, January 1, 2001; 142(1): 430 - 436. [Abstract] [Full Text] [PDF] |
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K.-S. Lee, H.-J. Kim, Q.-L. Li, X.-Z. Chi, C. Ueta, T. Komori, J. M. Wozney, E.-G. Kim, J.-Y. Choi, H.-M. Ryoo, et al. Runx2 Is a Common Target of Transforming Growth Factor beta 1 and Bone Morphogenetic Protein 2, and Cooperation between Runx2 and Smad5 Induces Osteoblast-Specific Gene Expression in the Pluripotent Mesenchymal Precursor Cell Line C2C12 Mol. Cell. Biol., December 1, 2000; 20(23): 8783 - 8792. [Abstract] [Full Text] |
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Y.-W. Zhang, N. Yasui, K. Ito, G. Huang, M. Fujii, J.-i. Hanai, H. Nogami, T. Ochi, K. Miyazono, and Y. Ito A RUNX2/PEBP2alpha A/CBFA1 mutation displaying impaired transactivation and Smad interaction in cleidocranial dysplasia PNAS, August 23, 2000; (2000) 180309597. [Abstract] [Full Text] |
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A. Yamaguchi, T. Komori, and T. Suda Regulation of Osteoblast Differentiation Mediated by Bone Morphogenetic Proteins, Hedgehogs, and Cbfa1 Endocr. Rev., August 1, 2000; 21(4): 393 - 411. [Abstract] [Full Text] [PDF] |
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W. Ishida, T. Hamamoto, K. Kusanagi, K. Yagi, M. Kawabata, K. Takehara, T. K. Sampath, M. Kato, and K. Miyazono Smad6 Is a Smad1/5-induced Smad Inhibitor. CHARACTERIZATION OF BONE MORPHOGENETIC PROTEIN-RESPONSIVE ELEMENT IN THE MOUSE Smad6 PROMOTER J. Biol. Chem., February 25, 2000; 275(9): 6075 - 6079. [Abstract] [Full Text] [PDF] |
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H. Watanabe, M. P. de Caestecker, and Y. Yamada Transcriptional Cross-talk between Smad, ERK1/2, and p38 Mitogen-activated Protein Kinase Pathways Regulates Transforming Growth Factor-beta -induced Aggrecan Gene Expression in Chondrogenic ATDC5 Cells J. Biol. Chem., April 20, 2001; 276(17): 14466 - 14473. [Abstract] [Full Text] [PDF] |
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S. Nishimori, Y. Tanaka, T. Chiba, M. Fujii, T. Imamura, K. Miyazono, T. Ogasawara, H. Kawaguchi, T. Igarashi, T. Fujita, et al. Smad-mediated Transcription Is Required for Transforming Growth Factor-beta 1-induced p57Kip2 Proteolysis in Osteoblastic Cells J. Biol. Chem., March 30, 2001; 276(14): 10700 - 10705. [Abstract] [Full Text] [PDF] |
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M. Izumi, Y. Fujio, K. Kunisada, S. Negoro, E. Tone, M. Funamoto, T. Osugi, Y. Oshima, Y. Nakaoka, T. Kishimoto, et al. Bone Morphogenetic Protein-2 Inhibits Serum Deprivation-induced Apoptosis of Neonatal Cardiac Myocytes through Activation of the Smad1 Pathway J. Biol. Chem., August 10, 2001; 276(33): 31133 - 31141. [Abstract] [Full Text] [PDF] |
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E. Piek, W. J. Ju, J. Heyer, D. Escalante-Alcalde, C. L. Stewart, M. Weinstein, C. Deng, R. Kucherlapati, E. P. Bottinger, and A. B. Roberts Functional Characterization of Transforming Growth Factor beta Signaling in Smad2- and Smad3-deficient Fibroblasts J. Biol. Chem., June 1, 2001; 276(23): 19945 - 19953. [Abstract] [Full Text] [PDF] |
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K. Pardali, A. Kurisaki, A. Moren, P. ten Dijke, D. Kardassis, and A. Moustakas Role of Smad Proteins and Transcription Factor Sp1 in p21Waf1/Cip1 Regulation by Transforming Growth Factor-beta J. Biol. Chem., September 15, 2000; 275(38): 29244 - 29256. [Abstract] [Full Text] [PDF] |
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Y.-W. Zhang, N. Yasui, K. Ito, G. Huang, M. Fujii, J.-i. Hanai, H. Nogami, T. Ochi, K. Miyazono, and Y. Ito A RUNX2/PEBP2alpha A/CBFA1 mutation displaying impaired transactivation and Smad interaction in cleidocranial dysplasia PNAS, September 12, 2000; 97(19): 10549 - 10554. [Abstract] [Full Text] [PDF] |
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