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Mouse (Murine) LDLR Protein expressed in Human Cells - ABIN2007638
Südhof, Goldstein, Brown, Russell: The LDL receptor gene: a mosaic of exons shared with different proteins. dans Science (New York, N.Y.) 1985
Show all 4 Pubmed References
Human LDLR Protein expressed in Wheat germ - ABIN1309277
Prunotto, Carnevali, Candiano, Murtas, Bruschi, Corradini, Trivelli, Magnasco, Petretto, Santucci, Mattei, Gatti, Scolari, Kador, Allegri, Ghiggeri: Autoimmunity in membranous nephropathy targets aldose reductase and SOD2. dans Journal of the American Society of Nephrology : JASN 2010
The frequency of known mutations in the LDLR gene in this cohort of patients was markedly low compared to frequencies reported in other populations.
This study adds 9 novel variations and 11 recurrent variations to the spectrum of LDLR gene mutations in Indian population. The in silico analysis for all the variations detected in this study were done to predict the probabilistic effect in pathogenicity of Familial Hypercholesterolemia.
Data suggest maternal glycemic response during pregnancy is associated with lower DNA methylation (Montrer HELLS Protéines) of 4 CpG sites within PDE4B (Montrer PDE4B Protéines) gene in placenta (collected after normal-weight term birth); 3 additional CpG sites are differentially methylated relative to maternal glucose response within TNFRSF1B (Montrer TNFRSF1B Protéines), LDLR, and BLM (Montrer BLM Protéines) genes. (PDE4B (Montrer PDE4B Protéines) = phosphodiesterase-4B; TNFRSF1B (Montrer TNFRSF1B Protéines) = TNF (Montrer TNF Protéines) receptor superfamily member-1B; BLM (Montrer BLM Protéines) = Bloom syndrome protein (Montrer BLM Protéines))
Vesicular stomatitis virus G protein complex with two distinct cysteine-rich domains (CR2 and CR3 (Montrer ITGAM Protéines)) of LDL-R
Report familial hypercholesterolemia patients with multiple mutations at the LDLR gene presenting with more severe phenotype than single mutants.
LDLr in the activated PSFs may become a novel target receptor for controlled drug delivery.
Systematic mutation of the AREs (ARE1-3) in the LDLR 3'UTR and expression of each mutant coupled to a luciferase reporter in Huh7 cells demonstrated that ARE1 is required for rapid LDLR mRNA decay and 5-AzaC-induced mRNA stabilization via the IRE1alpha-EGFR-ERK1/2 signaling cascade.
The genotype-risk associations were examined between LDLR (rs885765, rs688, rs5925, rs55903358, rs5742911) and obesity-related phenotypes and other comorbidities in Sucre, Venezuela. The association between LDLR rs5742911 ancestral genotype A/A and high risk condition related to HDL (Montrer HSD11B1 Protéines)-cholesterol was the only one found to be significant:(A/A: 41.50+/-14.81 mg/dL; A/G: 45.00+/-12.07 mg/dL; G/G: 47.17+/-9.43 mg/dL).
Heparan sulfate proteoglycans binding is required for PCSK9 (Montrer PCSK9 Protéines)-induced LDLR degradation.
membrane LDLR was reduced and lost the ability to take up LDL. Our data also expand the spectrum of known LDLR mutations
Nonesterified fatty acids significantly inhibit the expression of ApoB100 (Montrer APOB Protéines), ApoE (Montrer APOE Protéines), MTP (Montrer MTTP Protéines), and LDLR, thereby decreasing the synthesis and assembly of VLDL and inducing TG accumulation in bovine hepatocytes.
Platelet activation in ApoE (Montrer APOE Protéines) and LDLR-deficient mice was not further increased by strenuous exercise, but was instead attenuated.
Our data suggests that sphingosine-1-phosphate receptor 1 (Montrer S1PR1 Protéines) in macrophages plays an important role in protecting them against apoptosis in vitro and in atherosclerotic plaques in vivo, and delays diet induced atherosclerosis development in Ldlr deficient mice
Macrophage Fatp1 limits atherogenesis in LDL receptor knockout mice.
Network analysis reveals DJ-1 (Montrer PARK7 Protéines)/LDLR as common host proteins modulating pathogenesis of neurotropic viruses.
Atorvastatin therapy did not show cholesterol-independent effects on inflammation in atherosclerotic lesions in Ldlr(-/-)Apob(100 (Montrer APOB Protéines)/100) mice, whereas a cholesterol-lowering diet intervention was effective.
LDLR modulation is associated with early atherosclerosis-related lymphatic dysfunction, and bring forth a pleiotropic role for PCSK9 (Montrer PCSK9 Protéines) in lymphatic function.
FXR (Montrer NR1H4 Protéines) signaling is a bile acid nuclear receptor that regulates lipids and glucose homeostasis and lack of it causes hepatomegaly and liver dysfunction.
Endothelial LOX-1 (Montrer OLR1 Protéines) overexpression in an atherosclerosis-prone LDL receptor knockout mice impairs endothelial function, proving its importance in the development of atherosclerosis.
Dietary supplementation with the long chain monounsaturated fatty acid isomers C20:1 or C22:1 was equally effective in reducing atherosclerosis in LDLr(-/-)mice and this may partly occur through activation of the Ppar (Montrer PPARA Protéines) signaling pathways and favorable alterations in the proteome of lipoproteins.
Dihydromyricetin could reduce atherosclerosis via its pleiotropic effects, including improvement of endothelial dysfunction, inhibition of macrophage foam cell formation, amelioration of lipid profiles, anti-inflammatory action and anti-oxidative effect in LDL receptor deficient 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 (Montrer KLF13 Protéines) and SREBP-Sp1 (Montrer SP1 Protéines) activation interact to regulate low density lipoprotein receptor promoter function
found association between genotypes for LDLR and APOB (Montrer APOB Protéines) 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)