T
Takeyoshi Yamashita
Researcher at Kyowa Hakko Kirin Co., Ltd.
Publications - 50
Citations - 12168
Takeyoshi Yamashita is an academic researcher from Kyowa Hakko Kirin Co., Ltd.. The author has contributed to research in topics: Fibroblast growth factor 23 & Hypophosphatemia. The author has an hindex of 33, co-authored 50 publications receiving 11347 citations. Previous affiliations of Takeyoshi Yamashita include University of Tokyo.
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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.
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Increased circulatory level of biologically active full-length FGF-23 in patients with hypophosphatemic rickets/osteomalacia.
Yuji Yamazaki,Ryo Okazaki,Minako Shibata,Yukihiro Hasegawa,Kohei Satoh,Toshihiro Tajima,Yasuhiro Takeuchi,Toshiro Fujita,Kazuhiko Nakahara,Takeyoshi Yamashita,Seiji Fukumoto +10 more
TL;DR: It is likely that increased serum levels of FGF-23 contributes to the development of hypophosphatemia not only in TIO but also in XLH.