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Your search keyword '"Akiyama, Tetsu"' showing total 16 results
Start Over Author "Akiyama, Tetsu" Journal journal of biological chemistry
16 results on '"Akiyama, Tetsu"'

5. Crystal Structure of the Rac Activator, Asef, Reveals Its Autoinhibitory Mechanism

Author

Murayama, Kazutaka, primary, Shirouzu, Mikako, additional, Kawasaki, Yoshihiro, additional, Kato-Murayama, Miyuki, additional, Hanawa-Suetsugu, Kyoko, additional, Sakamoto, Ayako, additional, Katsura, Yasuhiro, additional, Suenaga, Atsushi, additional, Toyama, Mitsutoshi, additional, Terada, Takaho, additional, Taiji, Makoto, additional, Akiyama, Tetsu, additional, and Yokoyama, Shigeyuki, additional

Published
2007
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7. Wnt/β-Catenin and Estrogen Signaling Converge in Vivo

Author

Kouzmenko, Alexander P., primary, Takeyama, Ken-ichi, additional, Ito, Saya, additional, Furutani, Takashi, additional, Sawatsubashi, Shun, additional, Maki, Akio, additional, Suzuki, Eriko, additional, Kawasaki, Yoshihiro, additional, Akiyama, Tetsu, additional, Tabata, Testuya, additional, and Kato, Shigeaki, additional

Published
2004
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8. Identification of BMP and Activin Membrane-bound Inhibitor (BAMBI), an Inhibitor of Transforming Growth Factor-β Signaling, as a Target of the β-Catenin Pathway in Colorectal Tumor Cells

Author

Sekiya, Takashi, primary, Adachi, Shungo, additional, Kohu, Kazuyoshi, additional, Yamada, Tatsuya, additional, Higuchi, Osamu, additional, Furukawa, Yoichi, additional, Nakamura, Yusuke, additional, Nakamura, Tsutomu, additional, Tashiro, Kousuke, additional, Kuhara, Satoru, additional, Ohwada, Susumu, additional, and Akiyama, Tetsu, additional

Published
2004
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14. RICS, a Novel GTPase-activating Protein for Cdc42 and Rac1, Is Involved in the β-Catenin-N-cadherin and N-Methyl-D-aspartate Receptor Signaling.

Author

Okabe, Toshio, Nakamura, Tsutomu, Nishimura, Yukiko Nasu, Kohu, Kazuyoshi, Ohwada, Susumu, Morishita, Yasuo, and Akiyama, Tetsu

Subjects
*PROTEINS, *DENDRITIC cells
Abstract

Cites the involvement of a novel protein RICS in the beta-catenin-N-cadherin and n-methyl-D-aspartate receptor signaling. Role of cadherin adhesion molecules in the synaptic plasticity; Regulation of synaptic structure; Dendritic spine morphology regulation.

Published
2003
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15. The PX-RICS-14-3-3zeta/theta complex couples N-cadherin-beta-catenin with dynein-dynactin to mediate its export from the endoplasmic reticulum.

Author

Nakamura T, Hayashi T, Mimori-Kiyosue Y, Sakaue F, Matsuura K, Iemura S, Natsume T, and Akiyama T

Subjects
14-3-3 Proteins genetics, Animals, Antigens, CD genetics, COS Cells, Cadherins genetics, Chlorocebus aethiops, Dynactin Complex, Dyneins genetics, Endoplasmic Reticulum genetics, GTPase-Activating Proteins genetics, Gene Knockdown Techniques, HeLa Cells, Humans, Microtubule-Associated Proteins genetics, Microtubules genetics, Microtubules metabolism, Multiprotein Complexes genetics, Protein Transport physiology, beta Catenin genetics, cdc42 GTP-Binding Protein genetics, cdc42 GTP-Binding Protein metabolism, 14-3-3 Proteins metabolism, Antigens, CD metabolism, Cadherins metabolism, Dyneins metabolism, Endoplasmic Reticulum metabolism, GTPase-Activating Proteins metabolism, Microtubule-Associated Proteins metabolism, Multiprotein Complexes metabolism, beta Catenin metabolism
Abstract

We have recently shown that beta-catenin-facilitated export of cadherins from the endoplasmic reticulum requires PX-RICS, a beta-catenin-interacting GTPase-activating protein for Cdc42. Here we show that PX-RICS interacts with isoforms of 14-3-3 and couples the N-cadherin-beta-catenin complex to the microtubule-based molecular motor dynein-dynactin. Similar to knockdown of PX-RICS, knockdown of either 14-3-3zeta or - resulted in the disappearance of N-cadherin and beta-catenin from the cell-cell boundaries. Furthermore, we found that PX-RICS and 14-3-3zeta/ are present in a large multiprotein complex that contains dynein-dynactin components as well as N-cadherin and beta-catenin. Both RNAi- and dynamitin-mediated inhibition of dynein-dynactin function also led to the absence of N-cadherin and beta-catenin at the cell-cell contact sites. Our results suggest that the PX-RICS-14-3-3zeta/ complex links the N-cadherin-beta-catenin cargo with the dynein-dynactin motor and thereby mediates its endoplasmic reticulum export.

Published
2010
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16. Identification of BMP and activin membrane-bound inhibitor (BAMBI), an inhibitor of transforming growth factor-beta signaling, as a target of the beta-catenin pathway in colorectal tumor cells.

Author

Sekiya T, Adachi S, Kohu K, Yamada T, Higuchi O, Furukawa Y, Nakamura Y, Nakamura T, Tashiro K, Kuhara S, Ohwada S, and Akiyama T

Subjects
Adenoviridae genetics, Animals, Blotting, Northern, COS Cells, Carcinoma, Hepatocellular metabolism, Cell Line, Tumor, DNA Mutational Analysis, DNA-Binding Proteins metabolism, Dimerization, Genes, Reporter, Humans, Immunohistochemistry, Liver metabolism, Luciferases metabolism, Lymphoid Enhancer-Binding Factor 1, Membrane Proteins metabolism, Oligonucleotide Array Sequence Analysis, Plasmids metabolism, Promoter Regions, Genetic, Protein Structure, Tertiary, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Time Factors, Transcription Factors metabolism, Transcription, Genetic, Transcriptional Activation, Transforming Growth Factor beta antagonists & inhibitors, beta Catenin, Cell Membrane metabolism, Colorectal Neoplasms metabolism, Cytoskeletal Proteins metabolism, Membrane Proteins chemistry, Trans-Activators metabolism, Transforming Growth Factor beta metabolism
Abstract

The Wnt signaling pathway is activated in most human colorectal tumors. Mutational inactivation in the tumor suppressor adenomatous polyposis coli (APC), as well as activation of beta-catenin, causes the accumulation of beta-catenin, which in turn associates with the T cell factor/lymphoid enhancer factor (TCF/LEF) family of transcription factors and activates transcription of their target genes. Here we show that beta-catenin activates transcription of the BMP and activin membrane-bound inhibitor (BAMBI)/NMA gene. The expression level of BAMBI was found to be aberrantly elevated in most colorectal and hepatocellular carcinomas relative to the corresponding non-cancerous tissues. Expression of BAMBI in colorectal tumor cell lines was repressed by a dominant-negative mutant of TCF-4 or by an inhibitor of beta-catenin-TCF interaction, suggesting that beta-catenin is responsible for the aberrant expression of BAMBI in colorectal tumor cells. Furthermore, overexpression of BAMBI inhibited the response of tumor cells to transforming growth factor-beta signaling. These results suggest that beta-catenin interferes with transforming growth factor-beta-mediated growth arrest by inducing the expression of BAMBI, and this may contribute to colorectal and hepatocellular tumorigenesis.

Published
2004
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