PTHR - Parathyroid Hormone Receptor | Elisa - Clia - Antibody - Protein

Background

The Parathyroid Hormone Receptor (PTHR) is a G protein-coupled receptor (GPCR) that mediates the effects of parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP). PTHR is a class B GPCR that plays a central role in calcium homeostasis and bone metabolism by mediating the actions of parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP). PTHR is primarily expressed in bone, kidney, and parathyroid glands, where it regulates calcium and phosphate metabolism and bone remodeling. PTHR is activated by PTH, which is secreted by the parathyroid glands in response to low serum calcium levels. PTH stimulates bone resorption, renal calcium reabsorption, and the production of active vitamin D. PTHR also responds to PTHrP, a peptide with structural similarity to PTH. PTHrP regulates fetal calcium metabolism, skeletal development, and mammary gland function.In summary, the Parathyroid Hormone Receptor (PTHR) plays a critical role in calcium homeostasis, bone metabolism, and renal function by mediating the actions of parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP). Dysregulation of PTHR signaling is implicated in various metabolic bone disorders, highlighting its significance as a therapeutic target for conditions such as osteoporosis, hyperparathyroidism, and hypoparathyroidism.

Structural Features:

• PTHR belongs to the class B GPCR family and has a large extracellular N-terminal domain, seven transmembrane helices, and an intracellular C-terminal domain.
• Ligand binding induces conformational changes in the receptor, leading to activation of downstream signaling pathways.

Physiological Functions:

• Calcium Homeostasis: PTHR regulates serum calcium levels by modulating bone resorption, renal calcium reabsorption, and intestinal calcium absorption.
• Bone Remodeling: PTHR activation stimulates osteoclast activity and bone resorption, leading to the release of calcium and phosphate from bone.
• Renal Function: PTHR regulates renal calcium and phosphate handling, influencing urinary excretion and reabsorption of these minerals.

Clinical Implications:

• Hypoparathyroidism: Dysfunction of PTHR or deficiency of PTH can lead to hypoparathyroidism, characterized by low serum calcium levels, muscle cramps, and neuromuscular symptoms.
• Hyperparathyroidism: Overactivity of PTHR or excess PTH secretion can cause hyperparathyroidism, leading to hypercalcemia, kidney stones, and bone loss.
• Osteoporosis: Alterations in PTHR signaling contribute to bone loss and osteoporosis, a common age-related bone disorder.

Therapeutic Potential:

• PTH Analogs: Synthetic PTH analogs, such as teriparatide and abaloparatide, are used as anabolic agents for the treatment of osteoporosis by stimulating bone formation.
• PTHrP Analog: PTHrP analogs are being investigated for their potential therapeutic applications in conditions such as osteoporosis and bone fractures.
• PTHR Antagonists: PTHR antagonists are under development for the treatment of hyperparathyroidism, osteoporosis, and other bone disorders.