CASR
CASR (calcium sensing receptor, also known as GPRC2A, FHH, NSHPT, HHC and HHC1) is a plasma membrane G protein-coupled receptor that senses small changes in circulating calcium. It couples this signal to pathways controlling parathyroid hormone secretion and renal cation handling. Browse Assay Genie's current range of CASR research reagents below, or read on for the biology behind the target.
CASR is a G protein-coupled receptor that detects changes in the extracellular concentration of calcium ions and plays a key role in maintaining calcium homeostasis. It is activated by elevated circulating calcium, which leads to decreased parathyroid hormone (PTH) secretion in the parathyroid glands. In the kidneys, it acts as a key regulator of renal tubular calcium resorption. Activation follows a co-agonist mechanism: aromatic amino acids such as Trp or Phe act together with divalent cations such as calcium or magnesium to achieve full receptor activation.
Ligand binding causes a conformational change that triggers signalling through G proteins. Depending on context, the receptor couples to G(q)/G(11), G(i)/G(o) or G(s) classes. In the parathyroid and kidney it signals through G(q)/G(11) and G(i)/G(o): G(q)/G(11) coupling activates phospholipase C-beta, releasing the second messengers diacylglycerol and inositol 1,4,5-trisphosphate, while G(i)/G(o) coupling inhibits adenylate cyclase. Through G(i)/G(o) signalling and lower cAMP, CASR also activates the NLRP3 inflammasome by relieving cAMP-mediated inhibition. It further regulates the proton-sensing receptor GPR68 in a seesaw manner: CASR signalling inhibits GPR68 in response to extracellular calcium, whereas GPR68 inhibits CASR in the presence of extracellular protons.
The CASR gene encodes a protein of the G protein-coupled receptor 3 family and belongs to the HGNC group of calcium sensing receptors. Earlier names include hypocalciuric hypercalcemia 1 and calcium-sensing receptor. Mutations in the CASR gene cause familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism and autosomal dominant hypocalcemia, reflecting its essential role in mineral ion homeostasis.
CASR senses circulating calcium and is essential for maintaining mineral ion homeostasis.
Activation of CASR by elevated calcium decreases parathyroid hormone secretion in the parathyroid glands.
CASR acts as a key regulator of renal tubular calcium resorption and cation handling in the kidney.
CASR couples to several G protein classes and activates the NLRP3 inflammasome through G(i)/G(o)-mediated cAMP down-regulation.
CASR is a G protein-coupled receptor that senses extracellular calcium. When circulating calcium is high, it reduces parathyroid hormone secretion and regulates renal tubular calcium resorption. It signals through G(q)/G(11) and G(i)/G(o) proteins in the parathyroid and kidney, helping maintain calcium homeostasis.
CASR is also called GPRC2A, FHH, NSHPT, HHC and HHC1. Previous names include hypocalciuric hypercalcemia 1 and calcium-sensing receptor. UniProt lists the protein as extracellular calcium-sensing receptor, and it belongs to the G protein-coupled receptor 3 family.
Mutations in the CASR gene cause familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism and autosomal dominant hypocalcemia. Mouse and rat both have a Casr ortholog, so rodent models are used to study it. Check the datasheet of any product for its validated reactivity.
Pathway partners of CASR, including parathyroid hormone, GPR68 and NLRP3, with products at Assay Genie where available.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P41180; product specifications from Assay Genie datasheets.