Masayasu Yoshino
Astellas Pharma
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Publication
Featured researches published by Masayasu Yoshino.
Proceedings of the National Academy of Sciences of the United States of America | 2008
Mitsuyuki Matsumoto; Richard E. Straub; Stefano Marenco; Shun Ichiro Matsumoto; Akihiko Fujikawa; Sosuke Miyoshi; Miwako Shobo; Shinji Takahashi; Junko Yarimizu; Masatoshi Yuri; Masashi Hiramoto; Shuji Morita; Hiroyuki Yokota; Takeshi Sasayama; Kazuhiro Terai; Masayasu Yoshino; Joseph H. Callicott; Michael F. Egan; Andreas Meyer-Lindenberg; Lucas Kempf; Robyn Honea; Radha Krishna Vakkalanka; Jun Takasaki; Masazumi Kamohara; Takatoshi Soga; Hideki Hiyama; Hiroyuki Ishii; Ayako Matsuo; Shintaro Nishimura; Nobuya Matsuoka
The G protein-coupled receptor (GPCR) family is highly diversified and involved in many forms of information processing. SREB2 (GPR85) is the most conserved GPCR throughout vertebrate evolution and is expressed abundantly in brain structures exhibiting high levels of plasticity, e.g., the hippocampal dentate gyrus. Here, we show that SREB2 is involved in determining brain size, modulating diverse behaviors, and potentially in vulnerability to schizophrenia. Mild overexpression of SREB2 caused significant brain weight reduction and ventricular enlargement in transgenic (Tg) mice as well as behavioral abnormalities mirroring psychiatric disorders, e.g., decreased social interaction, abnormal sensorimotor gating, and impaired memory. SREB2 KO mice showed a reciprocal phenotype, a significant increase in brain weight accompanying a trend toward enhanced memory without apparent other behavioral abnormalities. In both Tg and KO mice, no gross malformation of brain structures was observed. Because of phenotypic overlap between SREB2 Tg mice and schizophrenia, we sought a possible link between the two. Minor alleles of two SREB2 SNPs, located in intron 2 and in the 3′ UTR, were overtransmitted to schizophrenia patients in a family-based sample and showed an allele load association with reduced hippocampal gray matter volume in patients. Our data implicate SREB2 as a potential risk factor for psychiatric disorders and its pathway as a target for psychiatric therapy.
FEBS Journal | 2010
Akira Suwa; Masayasu Yoshino; Chihiro Yamazaki; Masanori Naitou; Rie Fujikawa; Shunichiro Matsumoto; Takeshi Kurama; Teruhiko Shimokawa; Ichiro Aramori
The aim of this study is to discover and characterize novel energy homeostasis‐related molecules. We screened stock mouse embryonic stem cells established using the exchangeable gene trap method, and examined the effects of deficiency of the target gene on diet and genetic‐induced obesity. The mutant strain 0283, which has an insertion at the recQ‐mediated genome instability 1 (RMI1) locus, possesses a number of striking features that allow it to resist metabolic abnormalities. Reduced RMI1 expression, lower fasting‐blood glucose and a reduced body weight (normal diet) were observed in the mutant mice. When fed a high‐fat diet, the mutant mice were resistant to obesity, and also showed improved glucose intolerance and reduced abdominal fat tissue mass and food intake. In addition, the mutants were also resistant to obesity induced by the lethal yellow agouti (Ay) gene. Endogenous RMI1 genes were found to be up‐regulated in the liver and adipose tissue of KK‐Ay mice. RMI1 is a component of the Bloom’s syndrome gene helicase complex that maintains genome integrity and activates cell‐cycle checkpoint machinery. Interestingly, diet‐induced expression of E2F8 mRNA, which is an important cell cycle‐related molecule, was suppressed in the mutant mice. These results suggest that the regulation of energy balance by RMI1 is attributable to the regulation of food intake and E2F8 expression in adipose tissue. Taken together, these findings demonstrate that RMI1 is a novel molecule that regulates energy homeostasis.
Endocrine | 2011
Akira Suwa; Masayasu Yoshino; Takeshi Kurama; Teruhiko Shimokawa; Ichiro Aramori
RecQ-mediated genome instability 1 (RMI1) has been identified as a novel energy homeostasis-related molecule. While recent studies have suggested that change in RMI1 expression levels in adipose tissue may affect the body’s energy balance, no reports have identified the mechanism behind this expression regulation. In the present study, we found that RMI1 expression increased on differentiation of 3T3-L1 fibroblasts to adipocytes. In addition, glucose stimulation induced RMI1 expression to approximately eight times the baseline level. Further, knockdown of either E2F5 or E2F8 mRNA using siRNA suppressed this glucose-induced up-regulation of RMI1 expression. These results suggest that RMI1 expression may be regulated by glucose, at least in part, via E2F expression.
Genomics | 2006
Hitoshi Kato; Kyoko Nomura; Dai Osabe; Shuichi Shinohara; Osamu Mizumori; Rumi Katashima; Shoji Iwasaki; Koichi Nishimura; Masayasu Yoshino; Masato Kobori; Eiichiro Ichiishi; Naoto Nakamura; Toshikazu Yoshikawa; Toshihito Tanahashi; Parvaneh Keshavarz; Kiyoshi Kunika; Maki Moritani; Eiji Kudo; Kazue Tsugawa; Yoichiro Takata; Daisuke Hamada; Natsuo Yasui; Tatsuro Miyamoto; Hiroshi Shiota; Hiroshi Inoue; Mitsuo Itakura
Archive | 2013
Atsushi Suzuki; Makoto Asaumi; Kazuhisa Tsunoyama; Kouichi Nishimura; Akifumi Morinaka; Tomohiro Yamauchi; Masayasu Yoshino; Hiroaki Yoshizaki
Mammalian Genome | 2008
Takao Suzuki; Maki Moritani; Masayasu Yoshino; Mitsuhiro Kagami; Shoji Iwasaki; Kouichi Nishimura; Masahiko Akamatsu; Masato Kobori; Hitoshi Matsushime; Masao Kotoh; Kiyoshi Furuichi; Mitsuo Itakura
Archive | 2013
Atsushi Suzuki; Makoto Asaumi; Kazuhisa Tsunoyama; Kouichi Nishimura; Akifumi Morinaka; Tomohiro Yamauchi; Masayasu Yoshino; Hiroaki Yoshizaki
Archive | 2013
Atsushi Suzuki; Makoto Asaumi; Kazuhisa Tsunoyama; Kouichi Nishimura; Akifumi Morinaka; Tomohiro Yamauchi; Masayasu Yoshino; Hiroaki Yoshizaki
Archive | 2005
Mitsuo Itakura; Shoji Iwasaki; Masayasu Yoshino; Koichi Nishimuru
Archive | 2017
Akifumi Morinaka; Atsushi Suzuki; Hiroaki Yoshizaki; Kazuhisa Tsunoyama; Kouichi Nishimura; Makoto Asaumi; Masayasu Yoshino; Tomohiro Yamauchi