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Updated: Jan 17, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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Published on: February 28, 2017

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痕信号调节Fgf23表达通过交叉与缺氧和PTH途径在骨质细胞中的表达

Yoshihiro Tamamura1, Kenta Terai2, Akira Yamaguchi3

  • 1Department of Anatomy and Cell Biology, Institute of Biomedical Science, Tokushima University Graduate School, Tokushima, 770-8503, Japan; Oral Health Science Center, Tokyo Dental College, Tokyo, 101-0061, Japan.

Molecular and cellular endocrinology
|September 24, 2025
PubMed
概括

痕信号调节纤维细胞生长因子23 (Fgf23) 通过与缺氧和副甲状腺激素通路的相互作用来调节表达. 这项研究阐明了控制Fgf23的新机制,为相关骨疾病提供了潜在的治疗点.

关键词:
在 Fgf2323 中.低氧诱导因素是导致低氧的因素.在IDG-SW3细胞中,没有口,没有口.骨质细胞是一种骨质细胞.甲状腺上腺激素激素的作用蛋白激酶A是一种蛋白质激酶.在UMR-106细胞中,

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