K
Koichi Matsuda
Researcher at University of Tokyo
Publications - 362
Citations - 21946
Koichi Matsuda is an academic researcher from University of Tokyo. The author has contributed to research in topics: Genome-wide association study & Medicine. The author has an hindex of 65, co-authored 313 publications receiving 16523 citations. Previous affiliations of Koichi Matsuda include Vanderbilt University & Oklahoma Medical Research Foundation.
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Journal ArticleDOI
p53AIP1, a Potential Mediator of p53-Dependent Apoptosis, and Its Regulation by Ser-46-Phosphorylated p53
Katsutoshi Oda,Hirofumi Arakawa,Tomoaki Tanaka,Koichi Matsuda,Chizu Tanikawa,Toshiki Mori,Hiroyuki Nishimori,Katsuyuki Tamai,Takashi Tokino,Yusuke Nakamura,Yoichi Taya +10 more
TL;DR: The results suggest that p53AIP1 is likely to play an important role in mediating p53-dependent apoptosis, and phosphorylation of Ser-46 regulates the transcriptional activation of this apoptosis-inducing gene.
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ATF4 Is a Substrate of RSK2 and an Essential Regulator of Osteoblast Biology: Implication for Coffin-Lowry Syndrome
Xiangli Yang,Koichi Matsuda,Peter Bialek,Sylvie Jacquot,Howard C. Masuoka,Thorsten Schinke,Lingzhen Li,Stefano Brancorsini,Paolo Sassone-Corsi,Tim M. Townes,André Hanauer,Gerard Karsenty +11 more
TL;DR: This work identifies the transcription factor ATF4 as a critical substrate of RSK2 that is required for the timely onset of osteoblast differentiation, for terminal differentiation of osteoblasts, and for osteoplast-specific gene expression and indicates that lack of ATF4 phosphorylation by R SK2 may contribute to the skeletal phenotype of CLS.
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Histone Deacetylase 4 Controls Chondrocyte Hypertrophy during Skeletogenesis
Rick B. Vega,Koichi Matsuda,Junyoung Oh,Ana C. Barbosa,Xiangli Yang,Eric Meadows,John McAnally,Chris Pomajzl,John M. Shelton,James A. Richardson,Gerard Karsenty,Eric N. Olson +11 more
TL;DR: It is reported that HDAC4, which is expressed in prehypertrophic chondrocytes, regulates chONDrocyte hypertrophy and endochondral bone formation by interacting with and inhibiting the activity of Runx2, a transcription factor necessary for chondrosclerosis.
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Genome-wide association scan identifies a colorectal cancer susceptibility locus on 11q23 and replicates risk loci at 8q24 and 18q21.
Albert Tenesa,Susan M. Farrington,James G. D. Prendergast,Mary Porteous,Marion F Walker,Naila Haq,Rebecca A. Barnetson,Evropi Theodoratou,Roseanne Cetnarskyj,Nicola Cartwright,Colin A. Semple,Andrew G. Clark,Fiona Reid,Lorna Smith,Kostas Kavoussanakis,Thibaud Koessler,Paul D.P. Pharoah,Stephan Buch,Clemens Schafmayer,Jürgen Tepel,Stefan Schreiber,Henry Völzke,Carsten Oliver Schmidt,Jochen Hampe,Jenny Chang-Claude,Michael Hoffmeister,Hermann Brenner,Stefan Wilkening,Federico Canzian,Gabriel Capellá,Victor Moreno,Ian J. Deary,John M. Starr,Ian Tomlinson,Zoe Kemp,Kimberley Howarth,Luis G. Carvajal-Carmona,Emily L. Webb,Peter Broderick,Jayaram Vijayakrishnan,Richard S. Houlston,Gad Rennert,Dennis G. Ballinger,Laura S. Rozek,Stephen B. Gruber,Koichi Matsuda,Tomohide Kidokoro,Yusuke Nakamura,Brent W. Zanke,Brent W. Zanke,Brent W. Zanke,Celia M. T. Greenwood,Celia M. T. Greenwood,Jagadish Rangrej,Jagadish Rangrej,Rafal Kustra,Alexandre Montpetit,Thomas J. Hudson,Thomas J. Hudson,Steven Gallinger,Steven Gallinger,Harry Campbell,Malcolm G. Dunlop +62 more
TL;DR: Findings extend the understanding of the role of common genetic variation in CRC etiology by identifying a previously unreported association, rs3802842 on 11q23, and carrying all six possible risk alleles yielded OR = 2.6 (95% CI = 1.75–3.89) for CRC.
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A small-molecule AdipoR agonist for type 2 diabetes and short life in obesity
Miki Okada-Iwabu,Toshimasa Yamauchi,Masato Iwabu,Teruki Honma,Ken-ichi Hamagami,Koichi Matsuda,Mamiko Yamaguchi,Hiroaki Tanabe,Tomomi Kimura-Someya,Mikako Shirouzu,Hitomi Ogata,Kumpei Tokuyama,Kohjiro Ueki,Tetsuo Nagano,Akiko Tanaka,Shigeyuki Yokoyama,Takashi Kadowaki +16 more
TL;DR: AdipoRon showed very similar effects to adiponectin in muscle and liver, such as activation of AMPK and PPAR-α pathways, and ameliorated insulin resistance and glucose intolerance in mice fed a high-fat diet, and is a promising therapeutic approach for the treatment of obesity-related diseases such as type 2 diabetes.