Application Note
For ELISA: Use at a concentration of 0.5-1 μg/ml. For FACS: Use 5μg (undiluted) to label 10^6 clells - Incubate for 30min at 4oC. For ICC: Use at a dilution of 1-5 μg/ml. For IHC-Fr: Use at a dilution of 1-5 μg/ml. For IP: Use at a dilution of 1-2 μg/ml. For WB: Use at a dilution of 1-5 μg/ml. Predicted molecular weight: 160 kDa. Include 2mM Ca+2 with the antibody and avoid EDTA. Product GTX16897 has been reported to bind best to the unreduced LDL-R. Optimal dilutions/concentrations should be determined by the researcher.
Positive Control
Liver sections, HT1080 cells, HepG2 cells - Negative controls: HepG2 cells and normal skin
Form
Liquid
Buffer
50mM Sodium Phosphate, 0.2% Gelatin
Preservative
0.1% Sodium azide
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. Store at 4ºC. DO NOT FREEZE.
Concentration
0.1 mg/ml (Please refer to the vial label for the specific concentration.)
Antigen Species
Bovine
Immunogen
A trypic digest of low density lipoprotein receptor from bovine
Conjugation
Unconjugated
Note
For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.
Synonyms
Low Density Lipoprotein Receptor , Ldlr
Cellular Localization
Cell Membrane and Cytoplasmic
Background
The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. Low density lipoprotein (LDL) is normally bound at the cell membrane and taken into the cell ending up in lysosomes where the protein is degraded and the cholesterol is made available for repression of microsomal enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting step in cholesterol synthesis. At the same time, a reciprocal stimulation of cholesterol ester synthesis takes place. Mutations in this gene cause the autosomal dominant disorder, familial hypercholesterolemia.
Research Area