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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 Proteins (34) and many more products for this protein.
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This study demonstrated that IL-2 (show IL2 ELISA Kits) and IL-10 (show IL10 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) X(+) allele and ApoE (show APOE ELISA Kits) 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 ELISA Kits) may be important to identify patient's risk of CHD (show CHDH ELISA Kits), especially for female LDLR mutation carriers
Specifically, loss of IDOL (show MYLIP ELISA Kits) 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 ELISA Kits), ApoE (show APOE ELISA Kits), MTP (show MTTP ELISA Kits), 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 ELISA Kits)-deficient mice were much greater than in the Ldlr mice. These findings suggest that Apoe (show APOE ELISA Kits)-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 ELISA Kits) molecule (ApoB (show APOB ELISA Kits)-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 deficiency does not affect atherosclerosis development in LDLR knockout mice.
HDL (show HSD11B1 ELISA Kits) is redundant for adrenal steroidogenesis in LDLR knockout mice with a human-like lipoprotein profile
Neurometabolic roles of ApoE (show APOE ELISA Kits) and Ldl-R in mouse brain.
Absence of Elovl6 (show ELOVL6 ELISA Kits) attenuates steatohepatitis but promotes gallstone formation in a lithogenic diet-fed Ldlr(-/-) mouse model.
Suggest Idol (show MYLIP ELISA Kits) as a gatekeeper of LDLR-dependent ApoE (show APOE ELISA Kits) and Abeta (show APP ELISA Kits) clearance in the brain and a potential enzyme target for therapeutic intervention in Alzheimer disease.
binding of PCSK9 (show PCSK9 ELISA Kits) to GRP94 (show HSP90B1 ELISA Kits) protects LDLR from degradation likely by preventing early binding of PCSK9 (show PCSK9 ELISA Kits) 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 ELISA Kits) and SREBP-Sp1 (show SP1 ELISA Kits) activation interact to regulate low density lipoprotein receptor promoter function
found association between genotypes for LDLR and APOB (show APOB ELISA Kits) 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)