人甲状旁腺激素受体 1 抗体对
01AB03461
Parathyroid hormone 1 receptor (Parathyroid Hormone Receptor 1) is a class B G protein-coupled receptor primarily expressed in bone osteoblasts and the kidney, where it serves as a master regulator of calcium and phosphate homeostasis. The receptor consists of a large N-terminal extracellular domain for high-affinity ligand binding and a transmembrane domain that initiates intracellular signaling upon activation by parathyroid hormone or parathyroid hormone-related protein. Signaling occurs through Gs-mediated adenylyl cyclase activation and Gq-mediated phospholipase C pathways, ultimately promoting osteoclast-mediated bone resorption via RANKL upregulation. Clinically, constitutive activation of the receptor leads to Jansen's metaphyseal chondrodysplasia, while loss-of-function mutations are associated with Blomstrand chondrodysplasia and primary failure of tooth eruption. Due to its central role in bone remodeling, it is a major therapeutic target for the treatment of osteoporosis and hypoparathyroidism.
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技术参数
- 靶点基因名
- PTH1R
- 基因别名
- PTHR; PTHR1
- 蛋白别名
- parathyroid hormone 1 receptor; Parathyroid Hormone Receptor 1
- UniProt
- Q03431
- 物种
- Human
产品详情
- 靶点名称
- Parathyroid Hormone Receptor 1
- 蛋白名称
- parathyroid hormone 1 receptor
- 蛋白别名
- Parathyroid hormone/parathyroid hormone-related peptide receptor; PTH/PTHrP type I receptor; PTH/PTHr receptor; Parathyroid hormone 1 receptor; PTH1 receptor
- 靶点基因名
- PTH1R
- 基因别名
- PTHR; PTHR1
- UniProt
- Q03431
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Parathyroid hormone 1 receptor (Parathyroid Hormone Receptor 1) is a class B G protein-coupled receptor primarily expressed in bone osteoblasts and the kidney, where it serves as a master regulator of calcium and phosphate homeostasis. The receptor consists of a large N-terminal extracellular domain for high-affinity ligand binding and a transmembrane domain that initiates intracellular signaling upon activation by parathyroid hormone or parathyroid hormone-related protein. Signaling occurs through Gs-mediated adenylyl cyclase activation and Gq-mediated phospholipase C pathways, ultimately promoting osteoclast-mediated bone resorption via RANKL upregulation. Clinically, constitutive activation of the receptor leads to Jansen's metaphyseal chondrodysplasia, while loss-of-function mutations are associated with Blomstrand chondrodysplasia and primary failure of tooth eruption. Due to its central role in bone remodeling, it is a major therapeutic target for the treatment of osteoporosis and hypoparathyroidism.