Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. Additionally we are shipping LDLR Antibodies (244) and LDLR Kits (43) and many more products for this protein.
Showing 10 out of 34 products:
Mouse (Murine) LDLR Primary Antibody for - ABIN2007638
Südhof, Goldstein, Brown, Russell: The LDL receptor gene: a mosaic of exons shared with different proteins. in Science (New York, N.Y.) 1985
Show all 4 references for ABIN2007638
Human LDLR Primary Antibody for FACS - ABIN2666986
Bieghs, Van Gorp, Wouters, Hendrikx, Gijbels, van Bilsen, Bakker, Binder, Lütjohann, Staels, Hofker, Shiri-Sverdlov: LDL receptor knock-out mice are a physiological model particularly vulnerable to study the onset of inflammation in non-alcoholic fatty liver disease. in PLoS ONE 2012
Show all 4 references for ABIN2666986
Mouse (Murine) LDLR Primary Antibody for FACS - ABIN2666847
Brown, Goldstein: How LDL receptors influence cholesterol and atherosclerosis. in Scientific American 1985
Show all 4 references for ABIN2666847
Human LDLR Primary Antibody for - ABIN2181455
Nomura, Merched, Nour, Dieker, Oka, Chan: Low-density lipoprotein receptor gene therapy using helper-dependent adenovirus produces long-term protection against atherosclerosis in a mouse model of familial hypercholesterolemia. in Gene therapy 2004
This study demonstrated that IL-2 (show IL2 Proteins) and IL-10 (show IL10 Proteins) were related to gene polymorphisms of LDL-R, which might be involved in the development and progress of hypercholesterolemia.
Lipoprotein profiles get improved by liver-directed gene transfer of human LDLR gene in hypercholesterolaemia mice.
Multiple novel LDLR and ApoB (show APOB Proteins) mutations have been identified in a-United Kingdom-based cohort with familial hypercholesterolemia.
Mutations in LDLR is associated with coronary artery disease.
LDLR A(+)A(+) genotype, ApoB (show APOB Proteins) X(+) allele and ApoE (show APOE Proteins) E4 allele increased the risk of premature coronary artery disease by 1.8, 2.1 and 12.1 respectively.
The TT genotype of rs688 in the LDLR gene was not found to be associated with elevated levels of total cholesterol or LDL-C
Report increased intestinal cholesterol absorption and elevated serum cholesterol in families with primary hypercholesterolemia without mutations in LDLR.
genetic confirmation of ADH (show AVP Proteins) may be important to identify patient's risk of CHD (show CHDH Proteins), especially for female LDLR mutation carriers
Specifically, loss of IDOL (show MYLIP Proteins) increases LDLR distribution in the hepatic cell, and subsequently reduces serum LDL-C levels in dyslipidemic patients.
de novo mutation of the LDL receptor gene as the cause of familial hypercholesterolemia
Nonesterified fatty acids significantly inhibit the expression of ApoB100 (show APOB Proteins), ApoE (show APOE Proteins), MTP (show MTTP Proteins), and LDLR, thereby decreasing the synthesis and assembly of VLDL and inducing TG accumulation in bovine hepatocytes.
These data strongly imply that LDLr significantly contributes to beta-carotene uptake in the adult mouse liver. In contrast, LDLr does not seem to mediate acquisition of beta-carotene by the placental-fetal unit.
The values in the Apoe (show APOE Proteins)-deficient mice were much greater than in the Ldlr mice. These findings suggest that Apoe (show APOE Proteins)-deficient mice showed increased susceptibility to inflammation-associated colorectal carcinogenesis due to their high reactivity to inflammatory stimuli.
We carried out our experiment in mice deficient in the low density lipoprotein (LDL) receptor and expressing only ApoB100 (show APOB Proteins) molecule (ApoB (show APOB Proteins)-LDLr) where the development of atherosclerosis is known to closely mimic human atherosclerosis
Atherosclerosis is accelerated in LDL receptor-deficient mice fed a high-fat diet.
Myeloid cell IFNGR2 (show IFNGR2 Proteins) deficiency does not affect atherosclerosis development in LDLR knockout mice.
HDL (show HSD11B1 Proteins) is redundant for adrenal steroidogenesis in LDLR knockout mice with a human-like lipoprotein profile
Neurometabolic roles of ApoE (show APOE Proteins) and Ldl-R in mouse brain.
Absence of Elovl6 attenuates steatohepatitis but promotes gallstone formation in a lithogenic diet-fed Ldlr(-/-) mouse model.
Suggest Idol (show MYLIP Proteins) as a gatekeeper of LDLR-dependent ApoE (show APOE Proteins) and Abeta (show APP Proteins) clearance in the brain and a potential enzyme target for therapeutic intervention in Alzheimer disease.
binding of PCSK9 (show PCSK9 Proteins) to GRP94 (show HSP90B1 Proteins) protects LDLR from degradation likely by preventing early binding of PCSK9 (show PCSK9 Proteins) to LDLR
The LDLR gene should be a candidate causative gene for LDL-cholesterol and total cholesterol in pigs, but heterogeneity exists in different populations.
KLF13 (show KLF13 Proteins) and SREBP-Sp1 (show SP1 Proteins) activation interact to regulate low density lipoprotein receptor promoter function
found association between genotypes for LDLR and APOB (show APOB Proteins) polymorphisms and serum lipid levels, but none of them seem to be the causal mutation but probably represent closely linked polymorphisms
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. Alternate splicing results in multiple transcript variants.
low-density lipoprotein receptor
, LDL receptor
, low-density lipoprotein receptor class A domain-containing protein 3
, low density lipoprotein receptor (familial hypercholesterolemia)