K
Kohei Miyazono
Researcher at University of Tokyo
Publications - 520
Citations - 72948
Kohei Miyazono is an academic researcher from University of Tokyo. The author has contributed to research in topics: Transforming growth factor beta & Transforming growth factor. The author has an hindex of 135, co-authored 515 publications receiving 68706 citations. Previous affiliations of Kohei Miyazono include University of Tsukuba & University of Tokushima.
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Journal ArticleDOI
TGF-beta signalling from cell membrane to nucleus through SMAD proteins
TL;DR: Inhibitory SMADs have been identified that block the activation of these pathway-restricted SMADS that direct transcription to effect the cell's response to TGF-β.
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Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.
Masao Saitoh,Hideki Nishitoh,Makiko Fujii,Kohsuke Takeda,Kei Tobiume,Yasuhiro Sawada,Masahiro Kawabata,Kohei Miyazono,Hidenori Ichijo +8 more
TL;DR: Evidence that Trx is a negative regulator of ASK1 suggests possible mechanisms for redox regulation of the apoptosis signal transduction pathway as well as the effects of antioxidants against cytokine‐ and stress‐induced apoptosis.
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Induction of Apoptosis by ASK1, a Mammalian MAPKKK That Activates SAPK/JNK and p38 Signaling Pathways
Hidenori Ichijo,Eisuke Nishida,Kenji Irie,Peter ten Dijke,Masao Saitoh,Tetsuo Moriguchi,Minoru Takagi,Kunihiro Matsumoto,Kohei Miyazono,Yukiko Gotoh +9 more
TL;DR: Overexpression of ASK1 induced apoptotic cell death, andASK1 was activated in cells treated with tumor necrosis factor-α, and TNF-α-induced apoptosis was inhibited by a catalytically inactive form of AsK1.
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Accumulation of sub-100 nm polymeric micelles in poorly permeable tumours depends on size
Horacio Cabral,Yu Matsumoto,Kazue Mizuno,Qixian Chen,Mami Murakami,M. Kimura,Yasuko Terada,Mitsunobu R. Kano,Kohei Miyazono,Mitsuru Uesaka,Nobuhiro Nishiyama,Kazunori Kataoka +11 more
TL;DR: It is shown that the penetration and efficacy of the larger micelles could be enhanced by using a transforming growth factor-β inhibitor to increase the permeability of the tumours.
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ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis
Kei Tobiume,Atsushi Matsuzawa,Takumi Takahashi,Hideki Nishitoh,Kei Ichi Morita,Kohsuke Takeda,Osamu Minowa,Kohei Miyazono,Tetsuo Noda,Hidenori Ichijo +9 more
TL;DR: It is shown that by deleting ASK1 in mice, TNF‐ and H2O2‐induced sustained activations of JNK and p38 are lost inASK1−/− embryonic fibroblasts, and that ASK 1−-/− cells are resistant to TNF- and H1N1‐induced apoptosis.