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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
Heparan sulfate proteoglycans binding is required for PCSK9 (zeige PCSK9 Proteine)-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 (zeige FBXO8 Proteine)-depleted culture medium at the same levels as unmodified liposomes in FBS (zeige FBXO8 Proteine)-containing culture medium, which indicates that apolipoproteins A-I and E were the major serum components involved in liposomal binding to SR-B1 (zeige SCARB1 Proteine) or LDLR (or both).
These findings suggest that LDLR rs2738464 may affect the affinity of miR (zeige MLXIP Proteine)-330 binding to the LDLR 3'-UTR, thus regulating LDLR expression and contributing to clear cell renal cell carcinoma (zeige MOK Proteine) 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 (zeige ERBB2 Proteine)-overexpressing breast cancers in the setting of elevated circulating LDL cholesterol (LDL-C).
Identify LDLR, APOB (zeige APOB Proteine) and PCSK9 (zeige PCSK9 Proteine) 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.
PCSK9 (zeige PCSK9 Proteine) inhibits lipoprotein(a) clearance through the LDLR.
Nonesterified fatty acids significantly inhibit the expression of ApoB100 (zeige APOB Proteine), ApoE (zeige APOE Proteine), MTP (zeige MTTP Proteine), and LDLR, thereby decreasing the synthesis and assembly of VLDL and inducing TG accumulation in bovine hepatocytes.
Endothelial LOX-1 (zeige OLR1 Proteine) 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 (zeige PPARA Proteine) 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 (zeige HNRNPD Proteine) to accelerate LDLR mRNA degradation.
PPARdelta (zeige PPARD Proteine) activation attenuates hepatic steatosis in Ldlr-/- mice by enhanced fat oxidation, reduced lipogenesis, and improved insulin (zeige INS Proteine) sensitivity.
both LRP1 (zeige LRP1 Proteine) and LDLR expression and agLDL uptake are regulated by P2Y2R (zeige P2RY2 Proteine) in vascular smooth muscle cells, and agLDL uptake due to P2Y2R (zeige P2RY2 Proteine) activation is dependent upon cytoskeletal reorganization mediated by P2Y2R (zeige P2RY2 Proteine) binding to FLN-A (zeige FLNA Proteine)
this study shows that STAT4 (zeige STAT4 Proteine) regulates the CD8 (zeige CD8A Proteine)(+) regulatory T cell/T follicular helper cell axis and promotes atherogenesis in insulin (zeige INS Proteine)-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 (zeige APOE Proteine) allele (E4 versus E3) and docosahexaenoic acid intake. (APOE (zeige APOE Proteine) = apolipoprotein E (zeige APOE Proteine))
The LDLR gene should be a candidate causative gene for LDL-cholesterol and total cholesterol in pigs, but heterogeneity exists in different populations.
KLF13 (zeige KLF13 Proteine) and SREBP-Sp1 (zeige SP1 Proteine) activation interact to regulate low density lipoprotein receptor promoter function
found association between genotypes for LDLR and APOB (zeige APOB Proteine) 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)