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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
A randomized trial and novel SPR (Montrer SPR Protéines) technique identifies altered lipoprotein-LDL receptor binding as a mechanism underlying elevated LDL-cholesterol in APOE4s
Authors performed an analysis of public databases and literature for every variant published associated with FH, in the genes LDLR, APOB (Montrer APOB Protéines), and PCSK9 (Montrer PCSK9 Protéines).
In this review we present a broad spectrum of functionally characterized missense LDLr variants identified in patients with Familial hypercholesterolemia (FH), which is mandatory for a definite diagnosis of FH.
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.
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.
Vitamin D3 was a significantly beneficial dietary additive to blunt a prediabetic phenotype in diet-induced obesity of female LDLR(-/-) and LDLR(+/+) mice.
The results obtained from liver-specific NPC1L1 (Montrer NPC1L1 Protéines) transgenic mouse (L1-Tg) crossed with LDLR-/- mouse indicated no feedback mechanism to inhibit NPC1L1 (Montrer NPC1L1 Protéines) function in liver and hepatic expression of NPC1L1 (Montrer NPC1L1 Protéines) correlated with VLDL secretion in hypercholesterolemia state.
Type 2 diabetic, hyperlipidemic LDLr(-/-)ApoB(100 (Montrer APOB Protéines)/100) mice show increased calcific aortic valve disease.
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.
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)