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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 (228) and LDLR Proteins (27) and many more products for this protein.
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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
A recurrent frameshift mutation in LDLR gene causing familial hypercholesterolemia was identified in 9 probands and their relatives.
LDL receptor gene polymorphisms play a role in the treatment response of hepatitis C and the modulation of disease progression in Egyptians infected with chronic HCV.
This study aimed to perform a systematic review of LDLR mutations in China.
miR (show MLXIP ELISA Kits)-185 controls cholesterol homeostasis as a key posttranscriptional LDLR modulator in hepatic cells, providing novel insight into the regulatory mechanism for LDLR expression and the anti-atherosclerosis effect of miR (show MLXIP ELISA Kits)-185-inhibitor.
Three polymorphisms in the 3' UTR (show UTS2R ELISA Kits) region of LDLR, c.*52G>A, c.*504G>A, and c.*773A>G, and two at the 5' UTR (show UTS2R ELISA Kits) region of PCSK9 (show PCSK9 ELISA Kits), c.-3383C>G and c.-2063A>G, were associated with response to Armolipid Plus
in well characterized FCHL (show USF1 ELISA Kits) individuals, variants in LDLR and LPL (show LCP1 ELISA Kits) provide a small contribution to dyslipidemia
MicroRNA-27a has a role in decreasing the level and efficiency of the LDL receptor and contributes to the dysregulation of cholesterol homeostasis
Data suggest inducible expression of IDOL (show MYLIP ELISA Kits) is subject to robust, rapid regulation by process that is sensitive to deubiquitinase inhibition in human/mouse cell lines and primary human cells; transcriptional induction of IDOL (show MYLIP ELISA Kits) leads to degradation of LDLR.
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.
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
Short-term modulation of miR (show MLXIP ELISA Kits)-27b expression in wild-type mice regulates hepatic LDLR and ABCA1 (show ABCA1 ELISA Kits) expression but does not influence plasma and hepatic lipid levels.
The absence of PCSK9 (show PCSK9 ELISA Kits) results in a sex- and tissue-specific subcellular distribution of the LDLR and VLDLR (show VLDLR ELISA Kits), which is determined by estradiol levels.
In the present study, we examined the effects of H2 on atherosclerotic plaque stability and the underlying mechanisms in low-density lipoprotein receptor-knockout (LDLR-/-) mice and macrophage-derived foam cell models.
Targeted deletion of ChREBP (show MLXIPL ELISA Kits) in bone marrow cells resulted in accelerated atherosclerosis progression in Ldlr-/- mice with increased monocytosis, lesional macrophage accumulation, and plaque necrosis.
Blockade of Tim-1 (show HAVCR1 ELISA Kits) and Tim-4 (show TIMD4 ELISA Kits) enhances atherosclerosis in LDL receptor knockout mice.
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)