Human PTH1R Stable Cell Line - HEK293

Human parathyroid hormone 1 receptor (PTH1R), also known as PTHR1, is a class B G protein-coupled receptor activated by parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP) and biologically active amino-terminal fragments of these peptides. PTH1R is an important regulator of bone remodeling and systemic calcium and phosphate homeostasis. Upon ligand binding, the receptor can couple to Gαs, stimulating adenylyl cyclase, increasing intracellular cyclic AMP and activating protein kinase A. It can also engage Gαq-mediated phospholipase C signaling, leading to inositol phosphate formation, intracellular calcium mobilization and protein kinase C activation. PTH1R signaling is relevant to skeletal development, kidney function and mineral metabolism. Pathogenic variants in PTH1R have been associated with disorders including Jansen metaphyseal chondrodysplasia and Blomstrand chondrodysplasia, illustrating the consequences of abnormal receptor activation or loss of function.

The Human PTH1R Stable Cell Line - HEK293 is an engineered cell model that constitutively expresses human PTH1R in an adherent HEK293 background. It provides a consistent platform for examining receptor activation without the variability associated with repeated transient transfection. Functional assays may measure cAMP accumulation, CRE-dependent reporter activity, intracellular calcium mobilization, inositol phosphate production or other validated downstream responses. The cell line can be used to characterize PTH, PTHrP and related peptide analogues, generate concentration–response curves and compare the potency and efficacy of candidate agonists, antagonists or allosteric modulators. It may also support studies of ligand-biased signaling, receptor desensitization, internalization, β-arrestin recruitment and sustained signaling from intracellular compartments. These applications are relevant to early-stage drug discovery for bone and mineral disorders, including osteoporosis and hypoparathyroidism.