Zobrazeno 1 - 10
of 11
pro vyhledávání: '"Seiichiro Komatsu"'
Autor:
Hiroko Kokuba, Jun Takemura, Takashi Ishikawa, Kazuhiro Hirasawa, Keisuke Miyazawa, Masaki Hiramoto, Hiromi Kazama, Akihisa Abe, Shota Moriya, Ayako Hirota, Seiichiro Komatsu, Kana Miyahara
Publikováno v:
International Journal of Oncology
The ubiquitin-proteasome and autophagy-lysosome pathways are two major self-digestive systems for cellular proteins. Ubiquitinated misfolded proteins are degraded mostly by proteasome. However, when ubiquitinated proteins accumulate beyond the capaci
Autor:
Shota Moriya, Kaho Yamasaki, Akihiko Gotoh, Yusuke Kawai, Masaki Hiramoto, Keisuke Miyazawa, Seiichiro Komatsu, Masato Inazu, Ayako Hirota, Xiao-Fang Che, Hiroko Kokuba
Publikováno v:
International Journal of Oncology
The inhibitory effects of macrolide antibiotics including clarithromycin (CAM) on autophagy flux have been reported. Although a macrolide antibiotic exhibits no cytotoxicity, its combination with bortezomib (BZ), a proteasome inhibitor, for the simul
Autor:
Xiao-Fang Che, Shota Moriya, Keisuke Miyazawa, Seiichiro Komatsu, Norio Kohno, Tomohisa Yokoyama
Publikováno v:
Biochemical and Biophysical Research Communications. 437:41-47
The ubiquitin-proteasome pathway and the autophagy-lysosome pathway are two major intracellular protein degradation systems. We previously reported that clarithromycin (CAM) blocks autophagy flux, and that combined treatment with CAM and proteasome i
Autor:
Akihisa Abe, Akihiko Gotoh, Xiao-Fang Che, Masato Inazu, Keisuke Miyazawa, Tomohiro Kawaguchi, Akio Tomoda, Seiichiro Komatsu, Shota Moriya
Publikováno v:
International Journal of Oncology
The specific 26S proteasome inhibitor bortezomib (BZ) potently induces autophagy, endoplasmic reticulum (ER) stress and apoptosis in multiple myeloma (MM) cell lines (U266, IM-9 and RPMI8226). The macrolide antibiotics including concanamycin A, eryth
Autor:
Akiko Takase, Seiichiro Komatsu, Masahiro Itoh, Munekazu Naito, Masato Inazu, Keisuke Miyazawa, Shota Moriya, Akio Tomoda, Norio Kohno
Publikováno v:
International Journal of Oncology
The specific 26S proteasome inhibitor, bortezomib (BZ) potently induces apoptosis as well as autophagy in metastatic breast cancer cell lines such as MDA-MB-231 and MDA-MB-468. The combined treatment of clarithromycin (CAM) and BZ significantly enhan
Autor:
KANA MIYAHARA, HIROMI KAZAMA, HIROKO KOKUBA, SEIICHIRO KOMATSU, AYAKO HIROTA, JUN TAKEMURA, KAZUHIRO HIRASAWA, SHOTA MORIYA, AKIHISA ABE, MASAKI HIRAMOTO, TAKASHI ISHIKAWA, KEISUKE MIYAZAWA
Publikováno v:
International Journal of Oncology; Nov2016, Vol. 49 Issue 5, p1848-1858, 11p
Publikováno v:
Blood. 122:4910-4910
ER-stress is caused by an imbalance between the amount of unfolded or misfolded protein in the ER lumen and the capacity of the ER machinery to refold these proteins. This stress induces a coordinated cellular response known as unfolded protein respo
Autor:
Seiichiro Komatsu, Akihiko Gotoh, Tomohiro Kawaguchi, Shota Moriya, Akihisa Abe, Keisuke Miyazawa, Akio Tomoda, Masato Inazu, Xiao-Fang Che
Publikováno v:
Blood. 120:4992-4992
Abstract 4992 Macroautophagy (hereafter, “autophagy”) is a highly conserved cellular process of self-degradation in eukaryotes. Intracellular proteins and organelles including the endoplasmic reticulum (ER) are engulfed in a double-membrane vesic
Autor:
Shota Moriya, Masahiro Itoh, Norio Kohno, Munekazu Naito, Akiko Takase, Seiichiro Komatsu, Keisuke Miyazawa, Masato Inazu, Akio Tomoda
Publikováno v:
Cancer Research. 72:LB-157
Bortezomib (BZ), a selective and potent inhibitor of the 26S proteasome, has been approved for treating multiple myeloma. It was reported that BZ also inhibited breast cancer cell growth. Autophagy is a highly conserved cellular process in eukaryotes
Autor:
Hiroko Hayabe, Yoichi Osato, Akime Miyasato, Tetsuzo Tauchi, Kazuma Ohyashiki, Tomohisa Yokoyama, Takao Akashi, Seiichiro Komatsu
Publikováno v:
Cancer Research. 72:2275-2275
The BCR-ABL tyrosine kinase inhibitor (TKI), imatinib mesylate, has revolutionized the treatment of CML, however, the development of TKI-resistance caused in approximately 10-25% of cases by mutation in the BCR-ABL kinase domain. Therefore, novel the