H
Hiroshi I. Suzuki
Researcher at Massachusetts Institute of Technology
Publications - 76
Citations - 4904
Hiroshi I. Suzuki is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: microRNA & Regulation of gene expression. The author has an hindex of 32, co-authored 76 publications receiving 4075 citations. Previous affiliations of Hiroshi I. Suzuki include Nagoya University & University of Tokyo.
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Journal ArticleDOI
Modulation of microRNA processing by p53
Hiroshi I. Suzuki,Kaoru Yamagata,Koichi Sugimoto,Takashi Iwamoto,Shigeaki Kato,Kohei Miyazono +5 more
TL;DR: This study reveals a previously unrecognized function of p53 in miRNA processing, which may underlie key aspects of cancer biology, and suggests that transcription-independent modulation of miRNA biogenesis is intrinsically embedded in a tumour suppressive program governed by p53.
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MCPIP1 Ribonuclease Antagonizes Dicer and Terminates MicroRNA Biogenesis through Precursor MicroRNA Degradation
Hiroshi I. Suzuki,Mayu Arase,Hironori Matsuyama,Young Lim Choi,Toshihide Ueno,Hiroyuki Mano,Hiroyuki Mano,Koichi Sugimoto,Kohei Miyazono +8 more
TL;DR: The presence of this abortive processing machinery and diversity of MCPIP1-related genes may imply a dynamic evolutional transition of the RNA silencing system, and suggest that the balance between processing and destroying ribonucleases modulates miRNA biogenesis and potentially affects pathological miRNA dysregulation.
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Activin-Nodal signaling is involved in propagation of mouse embryonic stem cells.
Kazuya Ogawa,Akira Saito,Hisanori Matsui,Hiroshi I. Suzuki,Satoshi Ohtsuka,Daisuke Shimosato,Yasuyuki Morishita,Tetsuro Watabe,Hitoshi Niwa,Kohei Miyazono,Kohei Miyazono +10 more
TL;DR: It is suggested that endogenously activated autocrine loops of activin-Nodal signaling promote ES cell self-renewal.
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Super-Enhancer-Mediated RNA Processing Revealed by Integrative MicroRNA Network Analysis.
TL;DR: In this paper, super-enhancers drive the biogenesis of master miRNAs crucial for cell identity by enhancing both transcription and Drosha/DGCR8-mediated primary miRNA processing.
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miR-135b mediates NPM-ALK-driven oncogenicity and renders IL-17-producing immunophenotype to anaplastic large cell lymphoma.
Hironori Matsuyama,Hiroshi I. Suzuki,Hikaru Nishimori,Masaaki Noguchi,Takashi Yao,Norio Komatsu,Hiroyuki Mano,Hiroyuki Mano,Koichi Sugimoto,Kohei Miyazono +9 more
TL;DR: It is reported that microRNA-135b mediates nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)-driven oncogenicity and empowers IL-17-producing immunophenotype in anaplastic large cell lymphoma (ALCL) and reduces tumor angiogenesis and growth in vivo.