Anti-LDL antibody produced in chicken is suitable for indirect ELISA and western blotting analysis at a dilution of 1:500, for tissue or cell staining at a dilution of 1:200.
Biochem/physiol Actions
The Low-Density Lipoprotein (LDL) Receptor is a mosaic protein encoded by the LDLR gene in humans and belongs to the Low density lipoprotein receptor gene family. It is located on chromosome number 19. LDL receptor is a mosaic protein constituiting of exons shared with different proteins. It is crucial for cholesterol homeostasis and deficiency in LDLR functions leads to hypercholesterolemia. LDLR is a type I transmembrane protein that needs O-glycosylation for stable expression at the cell surface. Mutation in this gene may cause familial hypercholesterolemia (FH), which is an autosomal dominant disease.
Physical form
Solution in phosphate buffered saline containing 0.02% sodium azide.
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Proceedings of the National Academy of Sciences of the United States of America, 120(18), e2216668120-e2216668120 (2023-04-24)
Regulated cellular aggregation is an essential process for development and healing in many animal tissues. In some animals and a few distantly related unicellular species, cellular aggregation is regulated by diffusible chemical cues. However, it is unclear whether regulated cellular
GWAS have consistently revealed that LDLR locus variability influences LDL-cholesterol in general population. Severe LDLR mutations are responsible for familial hypercholesterolemia (FH). However, most primary hypercholesterolemias are polygenic diseases. Although Cis-regulatory regions might be the cause of LDL-cholesterol variability; an
The Journal of biological chemistry, 289(25), 17312-17324 (2014-05-07)
The low density lipoprotein receptor (LDLR) is crucial for cholesterol homeostasis and deficiency in LDLR functions cause hypercholesterolemia. LDLR is a type I transmembrane protein that requires O-glycosylation for stable expression at the cell surface. It has previously been suggested
Different types of immune cells are involved in atherogenesis and may act atheroprotective or atheroprogressive. Here, we describe an in vitro approach to analyze CD11c+ cells and CD11c+-derived ApoE in atherosclerosis. The major steps include harvesting mouse bone marrow, plating
Familial hypercholesterolemia (FH) is an autosomal dominant disease caused mainly by LDLR mutations. This study assessed the influence of the presence and type of LDLR mutation on lipid profile and the response to lipid-lowering therapy in Brazilian patients with heterozygous
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