CASR - Calcium Sensing Receptor | Elisa - Clia - Antibody - Protein

Background

The Calcium-sensing receptor (CASR) is a G protein-coupled receptor (GPCR) that plays a critical role in sensing extracellular calcium levels and regulating various physiological processes, including calcium homeostasis, bone metabolism, and hormone secretion. The primary endogenous ligand for CASR is extracellular calcium ions (Ca^2+). Additionally, CASR can be activated or modulated by other ions, such as magnesium (Mg^2+), amino acids, polyamines, and certain drugs.

Structural Features

CASR shares the characteristic seven-transmembrane domain structure typical of GPCRs. It consists of an extracellular N-terminus and an intracellular C-terminus, which interact with intracellular signaling molecules upon ligand binding. CASR activation leads to downstream signaling events mediated by heterotrimeric G proteins.

Physiological Functions

 CASR mediates various physiological effects in different tissues and organ systems:

• Calcium Homeostasis: CASR regulates extracellular calcium levels by modulating calcium reabsorption and excretion in the kidneys, calcium absorption in the intestines, and calcium release from bone.
• Parathyroid Hormone Regulation: CASR plays a crucial role in regulating parathyroid hormone (PTH) secretion in response to changes in extracellular calcium levels. Activation of CASR by high calcium levels inhibits PTH secretion, while low calcium levels stimulate PTH secretion.
• Bone Metabolism: CASR influences bone remodeling by regulating osteoblast and osteoclast activity, thus affecting bone mineral density and bone turnover.
• Hormone Secretion: CASR is expressed in various endocrine glands, including the parathyroid glands, thyroid gland, and adrenal glands, where it regulates hormone secretion in response to changes in extracellular calcium levels.

Clinical Implications:

 Dysregulation of CASR signaling is associated with various pathological conditions:

1. Hypercalcemia: Mutations or dysfunction of CASR may lead to hypercalcemia, a condition characterized by abnormally high levels of calcium in the blood.
2. Hypocalcemia: Altered CASR function may contribute to hypocalcemia, a condition characterized by abnormally low levels of calcium in the blood.
3. Hyperparathyroidism: Dysfunctional CASR signaling may result in primary hyperparathyroidism, a disorder characterized by excessive PTH secretion and hypercalcemia.
4. Osteoporosis: Changes in CASR activity may impact bone metabolism and contribute to the development of osteoporosis.

Therapeutic Potential

CASR represents a potential target for therapeutic intervention in calcium-related disorders and other diseases. Pharmacological modulation of CASR activity, either through allosteric modulators, agonists, or antagonists, holds promise for the development of novel therapies targeting this receptor.