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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
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
In Singapore, 52.1% (n=50) familial hypercholesterolemia had LDLR mutations, with 15 novel mutations found.
Investigated the role of Cys46 located in the first repeat of the LDL receptor binding domain in recognition of apolipoproteins. Functional characterization of p.(Cys46Gly) LDLR variant showed impaired LDL and VLDL binding and uptake activity.
Triglyceride-lowering LPL variants and LDL-C-lowering LDLR variants were associated with similar lower risk of CHD per unit difference in ApoB.
Letter: LDLR genotype is a significant determinant of the rebound in LDL-C concentration after LA among patients with homozygous familial hypercholesterolemia.
Mutation spectrum and genotype-phenotype correlation was analyzed in patients with familial hypercholesterolemia in Chinese population.
Knock down of FADS1 did not significantly change cholesterol efflux (p=0.70), but knockdown of INSIG1 and LDLR resulted in highly significant reduction of the efflux to HDL (67% and 75% of control, respectively, p<0.001).
Residual LDLR expression in homozygous familial hypercholesterolemia is a major determinant of LDL-C levels and seems to drive their individual response to evolocumab.
HepG2 cell lines transfected with siRNA directed to PCSK9 were challenged with Hcy, homocysteine thiolactone (HTL), testosterone, 5alpha-dihydroxytestosterone (5alpha-DHT), or estradiol for 24h, leading to an overt expression of PCSK9 and down-regulated expression of LDLR.
A randomized trial and novel SPR 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, and PCSK9.
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 of 4 CpG sites within PDE4B gene in placenta (collected after normal-weight term birth); 3 additional CpG sites are differentially methylated relative to maternal glucose response within TNFRSF1B, LDLR, and BLM genes. (PDE4B = phosphodiesterase-4B; TNFRSF1B = TNF receptor superfamily member-1B; BLM = Bloom syndrome protein)
Vesicular stomatitis virus G protein complex with two distinct cysteine-rich domains (CR2 and CR3) 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-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-induced LDLR degradation.
Nonesterified fatty acids significantly inhibit the expression of ApoB100, ApoE, MTP, and LDLR, thereby decreasing the synthesis and assembly of VLDL and inducing TG accumulation in bovine hepatocytes.
Therapy with pravastatin and cilostazol exerts beneficial effects by decreasing atherosclerotic lesion progression and improving the pro-inflammatory state in the vascular endothelium of LDL receptor knockout mice.
Data suggest that expression of Pcsk9 and Ldlr in liver and pancreas can be regulated by dietary measures; here, dietary supplementation with quercetin-3-glucoside modulates expression of Pcsk9 and Ldlr in prevention of hyperlipidemia and hyperinsulinemia induced by high dietary cholesterol. (Pcsk9 = proprotein convertase subtilisin/kexin type-9; Ldlr = low-density lipoprotein receptor)
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 transgenic mouse (L1-Tg) crossed with LDLR-/- mouse indicated no feedback mechanism to inhibit NPC1L1 function in liver and hepatic expression of NPC1L1 correlated with VLDL secretion in hypercholesterolemia state.
Type 2 diabetic, hyperlipidemic LDLr(-/-)ApoB(100/100) mice show increased calcific aortic valve disease.
Platelet activation in ApoE and LDLR-deficient mice was not further increased by strenuous exercise, but was instead attenuated.
Our data suggests that sphingosine-1-phosphate receptor 1 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/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(100/100) 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 in lymphatic function.
FXR 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 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 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.
data reveal a novel role of Ldlr as functional modulator of metabolic alterations associated with hypogonadism.
this work identifies a novel posttranscriptional regulatory mechanism by which dietary cholesterol inhibits liver LDLR expression via inducing HNRNPD to accelerate LDLR mRNA degradation.
PPARdelta activation attenuates hepatic steatosis in Ldlr-/- mice by enhanced fat oxidation, reduced lipogenesis, and improved insulin sensitivity.
both LRP1 and LDLR expression and agLDL uptake are regulated by P2Y2R in vascular smooth muscle cells, and agLDL uptake due to P2Y2R activation is dependent upon cytoskeletal reorganization mediated by P2Y2R binding to FLN-A
Results indicate the importance of the LDL receptor (LDLR) in the growth of triple-negative and HER2-overexpressing breast cancers in the setting of elevated circulating LDL cholesterol (LDL-C).
The LDLR gene should be a candidate causative gene for LDL-cholesterol and total cholesterol in pigs, but heterogeneity exists in different populations.
KLF13 and SREBP-Sp1 activation interact to regulate low density lipoprotein receptor promoter function
found association between genotypes for LDLR and APOB 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)