T
Takashi Shimada
Researcher at Nippon Medical School
Publications - 218
Citations - 15059
Takashi Shimada is an academic researcher from Nippon Medical School. The author has contributed to research in topics: Genetic enhancement & Gene. The author has an hindex of 50, co-authored 213 publications receiving 14015 citations. Previous affiliations of Takashi Shimada include Kitasato University.
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Journal ArticleDOI
Klotho converts canonical FGF receptor into a specific receptor for FGF23
Itaru Urakawa,Yuji Yamazaki,Takashi Shimada,Kousuke Iijima,Hisashi Hasegawa,Katsuya Okawa,Toshiro Fujita,Seiji Fukumoto,Takeyoshi Yamashita +8 more
TL;DR: It is shown that a previously undescribed receptor conversion by Klotho, a senescence-related molecule, generates the FGF23 receptor, and insights into the diversity and specificity of interactions between FGF and FGF receptors are provided.
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FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis.
Takashi Shimada,Hisashi Hasegawa,Yuji Yamazaki,Takanori Muto,Rieko Hino,Yasuhiro Takeuchi,Toshiro Fujita,Kazuhiko Nakahara,Seiji Fukumoto,Takeyoshi Yamashita +9 more
TL;DR: FGF‐23 is a potent regulator of the vitamin D and phosphate metabolism and caused a reduction in serum 1,25‐dihydroxyvitamin D by altering the expressions of key enzymes for the vitaminD metabolism followed by hypophosphatemia.
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Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism
Takashi Shimada,Makoto Kakitani,Yuji Yamazaki,Hisashi Hasegawa,Yasuhiro Takeuchi,Toshiro Fujita,Seiji Fukumoto,Kazuma Tomizuka,Takeyoshi Yamashita +8 more
TL;DR: Evidence is presented that FGF23 is a physiological regulator of serum phosphate and 1,25-dihydroxyvitamin D (1,25[OH]2D) by generating FGF 23-null mice, indicating that F GF23 is essential for normal phosphate and vitamin D metabolism.
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Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia
Takashi Shimada,Satoru Mizutani,Takanori Muto,Takashi Yoneya,Rieko Hino,Shu Takeda,Yasuhiro Takeuchi,Toshiro Fujita,Seiji Fukumoto,Takeyoshi Yamashita +9 more
TL;DR: It is concluded that overproduction of F GF23 causes TIO, whereas mutations in the FGF23 gene result in autosomal dominant hypophosphatemic rickets possibly by preventing proteolytic cleavage and enhancing biological activity of FGF 23.
Journal ArticleDOI
Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo.
Takashi Shimada,Takanori Muto,Itaru Urakawa,Takashi Yoneya,Yuji Yamazaki,Katsuya Okawa,Yasuhiro Takeuchi,Toshiro Fujita,Seiji Fukumoto,Takeyoshi Yamashita +9 more
TL;DR: It is concluded that ADHR is caused by hypophosphatemic action of mutant full-length FGF-23 proteins that are resistant to the cleavage between Arg(179) and Ser(180).