Rat Calcitonin Receptor (CALCR) Protein

Background

Calcitonin Receptor (CALCR) is a G-protein-coupled receptor that mediates the actions of calcitonin, a hormone primarily involved in calcium homeostasis and bone metabolism. CALCR is predominantly expressed in osteoclasts, where it inhibits bone resorption by reducing osteoclast activity and survival, thus maintaining bone mineral density. This function is critical for conditions like osteoporosis, where dysregulated bone turnover leads to bone fragility. Beyond bone health, CALCR is also expressed in the kidneys, where it enhances renal calcium excretion to regulate systemic calcium levels. Additionally, CALCR signaling in the central nervous system influences appetite regulation and energy metabolism, providing potential roles in managing obesity and metabolic disorders. CALCR is activated not only by calcitonin but also by related peptides, such as amylin, which are involved in glucose homeostasis and insulin secretion. Importantly, CALCR has been implicated in cancer progression, particularly in bone metastasis, where calcitonin receptor expression correlates with increased osteoclast activity and skeletal degradation. Dysregulation of CALCR signaling is also associated with diseases like Paget's disease and hypercalcemia of malignancy, where excessive calcium release disrupts homeostasis. Therapeutically, calcitonin analogs and CALCR-targeted drugs are widely used for treating osteoporosis, hypercalcemia, and bone pain. Emerging research suggests that CALCR may have broader roles in cardiovascular and neurodegenerative conditions, further underscoring its biological versatility and therapeutic potential.