Tadashi Matsuda
Research Subjects
Tadashi Matsuda has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
Atsushi Muraguchi
From the ‡Department of Immunology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan, and the ‖Biotechnology Center of Oslo, University of Oslo, Gaustadalleen 21, Oslo 0349, Norway
3 shared publicationsTetsuya Yamamoto
From the ‡Department of Immunology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan, and the ‖Biotechnology Center of Oslo, University of Oslo, Gaustadalleen 21, Oslo 0349, Norway
3 shared publicationsHiroyuki Kishi
2 shared publicationsAkihiko Yoshimura
1 shared publicationAkira Junicho
1 shared publicationFahri Saatcioglu
1 shared publication
Latest Publications
- Open Access
- 1 November 2001
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 276 (46) , 42908-42914
Cross-talk between Transforming Growth Factor-β and Estrogen Receptor Signaling through Smad3
- 1 November 2001
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 276 (46) , 42908-42914
Open AccessCross-talk between Transforming Growth Factor-β and Estrogen Receptor Signaling through Smad3
- 1 April 2001
- Published by Elsevier in Biochemical and Biophysical Research Communications
- Vol. 283 (1) , 179-187
Cross-Talk between Signal Transducer and Activator of Transcription 3 and Androgen Receptor Signaling in Prostate Carcinoma Cells
- 1 April 2001
- Published by Elsevier in Biochemical and Biophysical Research Communications
- Vol. 283 (1) , 179-187
Cross-Talk between Signal Transducer and Activator of Transcription 3 and Androgen Receptor Signaling in Prostate Carcinoma Cells
- 27 April 2000
- Published by Wiley in FEBS Letters
- Vol. 472 (2-3) , 235-240
SOCS‐1 can suppress CD3ζ‐ and Syk‐mediated NF‐AT activation in a non‐lymphoid cell line
To elucidate T cell antigen receptor (TCR) signaling leading to activation nuclear factor of activated T cells (NF‐AT), we reconstituted TCR signaling to activate NF‐AT in a non‐lymphoid cell line, 293T. We demonstrated that co‐expression of CD8/ζ and Syk were necessary for NF‐AT activation in 293T. This NF‐AT response was completely inhibited by the addition of cyclosporin A or FK506, but markedly enhanced by the additional expression of Tec protein tyrosine kinase. We also show that the cytokine signaling suppressor, suppressor of cytokine signaling 1, potently inhibited this response by interacting with Syk and immunoreceptor tyrosine‐based activation motifs in CD8/ζ. These results imply that this novel system may provide a useful tool to delineate or identify the regulatory molecules for CD3ζ/Syk‐mediated NF‐AT activation.
- 27 April 2000
- Published by Wiley in FEBS Letters
- Vol. 472 (2-3) , 235-240
SOCS‐1 can suppress CD3ζ‐ and Syk‐mediated NF‐AT activation in a non‐lymphoid cell line
To elucidate T cell antigen receptor (TCR) signaling leading to activation nuclear factor of activated T cells (NF‐AT), we reconstituted TCR signaling to activate NF‐AT in a non‐lymphoid cell line, 293T. We demonstrated that co‐expression of CD8/ζ and Syk were necessary for NF‐AT activation in 293T. This NF‐AT response was completely inhibited by the addition of cyclosporin A or FK506, but markedly enhanced by the additional expression of Tec protein tyrosine kinase. We also show that the cytokine signaling suppressor, suppressor of cytokine signaling 1, potently inhibited this response by interacting with Syk and immunoreceptor tyrosine‐based activation motifs in CD8/ζ. These results imply that this novel system may provide a useful tool to delineate or identify the regulatory molecules for CD3ζ/Syk‐mediated NF‐AT activation.