LDLR
LDLR (low density lipoprotein receptor, also listed as LDLCQ2) is a cell surface receptor that mediates receptor-mediated endocytosis of specific ligands, notably low density lipoprotein and cholesterol. It belongs to the LDLR family and is linked to familial hypercholesterolemia. Browse Assay Genie's current range of LDLR research reagents below, or read on for the biology behind the target.
LDLR is a cell surface protein that takes part in receptor-mediated endocytosis. At the cell membrane it binds low density lipoprotein (LDL) and cholesterol, and the bound ligand is taken into the cell. Lysosomes then release the cholesterol, which becomes available to repress microsomal 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting enzyme of cholesterol synthesis. In parallel, cholesterol ester synthesis is stimulated reciprocally. This makes the receptor a central link between lipoprotein uptake and the control of intracellular cholesterol production.
The human protein is annotated at the cell membrane and in clathrin-coated pits, and it is also found in the Golgi apparatus, early and late endosomes and lysosomes, reflecting its trafficking through the endocytic pathway. LDLR belongs to the LDLR family, a group of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. The HGNC places the gene in the low density lipoprotein receptors group and also among microRNA protein coding host genes. The mouse and rat orthologs are both named Ldlr, so the receptor is accessible in common rodent models. The NCBI Gene summary notes that alternate splicing of the LDLR gene gives rise to multiple transcript variants.
Mutations in the LDLR gene cause the autosomal dominant disorder familial hypercholesterolemia, which is why the receptor is so widely studied in lipid biology. UniProt additionally records that LDLR acts as a receptor for many alphaviruses, including Getah virus, Ross river virus and Semliki Forest virus, giving it relevance in microbial infection research as well as in cholesterol metabolism.
LDLR binds LDL and cholesterol for uptake, and the released cholesterol represses HMG CoA reductase, making it central to studies of cholesterol homeostasis.
Mutations in the LDLR gene cause autosomal dominant familial hypercholesterolemia, so the receptor is a core subject in genetic lipid disorder studies.
LDLR moves from clathrin-coated pits through early and late endosomes to lysosomes, a route used to study receptor-mediated endocytosis.
LDLR acts as a receptor for several alphaviruses, including Getah virus, Ross river virus and Semliki Forest virus, supporting infection biology research.
LDLR is a cell surface receptor that binds low density lipoprotein and cholesterol and brings them into the cell by endocytosis. Lysosomes release the cholesterol, which represses HMG CoA reductase, the rate-limiting enzyme of cholesterol synthesis. It also serves as a receptor for several alphaviruses.
The approved HGNC name is low density lipoprotein receptor, and LDLCQ2 is a listed alias. UniProt names the protein low-density lipoprotein receptor. According to the NCBI Gene summary, alternate splicing of the LDLR gene produces multiple transcript variants.
Yes. Mutations in the LDLR gene cause autosomal dominant familial hypercholesterolemia. Orthologs named Ldlr exist in both mouse and rat, so rodent models are commonly used; check the datasheet of any product for its validated reactivity.
Other members of the LDLR-related protein group with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P01130; product specifications from Assay Genie datasheets.