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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. in 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. in Science (New York, N.Y.) 1985
Show all 4 Pubmed References
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 (show HSD11B1 Proteins)-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 (show PCSK9 Proteins)-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
Liposomes modified with both apolipoproteins A-I and E were internalized in HepG2 cells in FBS (show FBXO8 Proteins)-depleted culture medium at the same levels as unmodified liposomes in FBS (show FBXO8 Proteins)-containing culture medium, which indicates that apolipoproteins A-I and E were the major serum components involved in liposomal binding to SR-B1 (show SCARB1 Proteins) or LDLR (or both).
These findings suggest that LDLR rs2738464 may affect the affinity of miR (show MLXIP Proteins)-330 binding to the LDLR 3'-UTR, thus regulating LDLR expression and contributing to clear cell renal cell carcinoma (show MOK Proteins) risk
the p.(Gly20Arg) change in the LDL receptor, previously described as disease causing, has no detrimental effect on protein expression or LDL particle binding
Twenty mutations including synonymous, missense, and intronic mutations were identified in the LDLR coding region of 32 Brazilian patients with familial hypercholesterolemia.
Results indicate the importance of the LDL receptor (LDLR) in the growth of triple-negative and HER2 (show ERBB2 Proteins)-overexpressing breast cancers in the setting of elevated circulating LDL cholesterol (LDL-C).
Identify LDLR, APOB (show APOB Proteins) and PCSK9 (show PCSK9 Proteins) novel mutations causing familial hypercholesterolemia in the central south region of China.
This study updates the LDLR variant database and identifies a number of reported variants of unknown significance where additional family and in vitro studies will be required to confirm or refute their pathogenicity.
Nonesterified fatty acids significantly inhibit the expression of ApoB100 (show APOB Proteins), ApoE (show APOE Proteins), MTP (show MTTP Proteins), and LDLR, thereby decreasing the synthesis and assembly of VLDL and inducing TG accumulation in bovine hepatocytes.
Endothelial LOX-1 (show OLR1 Proteins) 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 (show PPARA Proteins) 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 (show HNRNPD Proteins) to accelerate LDLR mRNA degradation.
PPARdelta (show PPARD Proteins) activation attenuates hepatic steatosis in Ldlr-/- mice by enhanced fat oxidation, reduced lipogenesis, and improved insulin (show INS Proteins) sensitivity.
both LRP1 (show LRP1 Proteins) and LDLR expression and agLDL uptake are regulated by P2Y2R (show P2RY2 Proteins) in vascular smooth muscle cells, and agLDL uptake due to P2Y2R (show P2RY2 Proteins) activation is dependent upon cytoskeletal reorganization mediated by P2Y2R (show P2RY2 Proteins) binding to FLN-A (show FLNA Proteins)
this study shows that STAT4 (show STAT4 Proteins) regulates the CD8 (show CD8A Proteins)(+) regulatory T cell/T follicular helper cell axis and promotes atherogenesis in insulin (show INS Proteins)-resistant Ldlr(-/-) mice
Data (including data from studies using transgenic mice) suggest that plasma and liver cholesterol homeostasis and hepatic expression of LDL receptor and lipolysis-stimulated lipoprotein receptor are modulated differently and independently by APOE (show APOE Proteins) allele (E4 versus E3) and docosahexaenoic acid intake. (APOE (show APOE Proteins) = apolipoprotein E (show APOE Proteins))
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 Proteins) and SREBP-Sp1 (show SP1 Proteins) activation interact to regulate low density lipoprotein receptor promoter function
found association between genotypes for LDLR and APOB (show APOB Proteins) 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)