Rat LDLR(Low Density Lipoprotein Receptor) ELISA Kit (E-EL-R2584)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Rat LDLR. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Rat LDLR and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Rat LDLR, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Rat LDLR. You can calculate the concentration of Rat LDLR in the samples by comparing the OD of the samples to the standard curve.

The Low-Density Lipoprotein Receptor (LDLR) is the founding member of the LDLR family of widely expressed cell surface scavenger receptors . Many proteins in the LDLR family are cleaved by extracellular proteases to release soluble forms into the circulation, and many of these soluble forms are active . Mature LDLR is a 160 kDa type I transmembrane glycoprotein that contains cysteine-rich complement-like repeats (class A LDLR domains), calcium-binding EGF repeats, and β-propeller structures (class B LDLR domains) in the ECD. LDLR is constitutively and widely expressed. Its expression can be downregulated by LDL and upregulated by hormones such as insulin and estradiol, and by many cytokines. Hepatocyte LDLR is responsible for endocytosis and clearing of most plasma LDL cholesterol. LDLR binds the ApoB portion of LDL and brings it into endocytic vesicles. It dissociates at the low pH of the vesicle, allowing LDL to be degraded while LDLR is recycled back to the cell surface. Lack of LDLR expression or function causes familial hypercholesterolemia (FH); over 1100 FH-related LDLR mutations have been identified. Overexpression or hyperfunction of the protease PCSK9 can also cause increased plasma cholesterol by lowering cell surface LDLR expression.PCSK9 alters the pH-induced LDLR conformation change in the endocytic vesicle, thus promoting LDLR degradation rather than recycling to the cell surface .