Leptin Responsive Luciferase Reporter HEK293 Cell Line

The Leptin Responsive Luciferase Reporter HEK293 Cell Line a HEK293 cell line that expresses the full-length human leptin receptor (NM_002303.6) under the control of a CMV promoter for high constitutive expression, and an inducible firefly luciferase reporter controlled by the STAT3 Response Element located upstream of a minimal TATA promoter. Upon leptin-ligand binding, the leptin receptor will activate the STAT3 signaling pathway, leading to expression of the STAT3-controlled luciferase reporter. This cell line has been validated by stimulation with leptin and with the leptin receptor agonist antibody, Mibavademab. Figure 1: Illustration of the mechanism leading to luciferase induction upon leptin treatment in Leptin Responsive Luciferase Reporter HEK293 Cell Line. Interested in screening and profiling inhibitors, blocking antibodies, or activators leptin receptor without the need to purchase and license the cell line? Check out our Cell Signaling Pathway Screening. Leptin is a hormone primarily produced by fat cells (adipocytes) that regulates appetite and energy balance by acting on receptors in the brain's hypothalamus. High levels of leptin signal to the brain that fat stores are sufficient, reducing appetite and increasing energy expenditure, whereas low levels stimulate appetite. A disruption in this system, either through a lack of leptin or resistance to it, is linked to several diseases, most notably obesity. Congenital leptin deficiency (CLD) is a rare genetic disorder caused by mutations in the leptin gene, resulting in a complete lack of leptin. This leads to severe, early-onset obesity due to constant hunger (hyperphagia). Other symptoms include hypogonadotropic hypogonadism, which causes delayed or absent puberty. Leptin resistance is a more common condition seen in most people with obesity. Despite high circulating leptin levels, the body becomes less sensitive to the hormone, causing the satiety signal to fail, which contributes to continued overeating and weight gain. This is strongly linked to metabolic disorders, including Type 2 diabetes (T2D), hypertension, cardiovascular disease, and nonalcoholic fatty liver disease (MASH).