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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. in 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. in Journal of the American Society of Nephrology : JASN 2010
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.
4 siblings found to be compound heterozygotes for 2 LDLR gene mutations but showing a different phenotype severity
LDLR is a relevant receptor for CNS drug delivery via receptor-mediated transcytosis and that the peptide vectors we developed have the potential to transport drugs
Higher Gleason grade was associated with lower LDLR expression, lower SOAT1 (zeige SOAT1 Proteine) and higher SQLE (zeige SQLE Proteine) expression. Besides high SQLE (zeige SQLE Proteine) expression, cancers that became lethal despite primary treatment were characterized by low LDLR expression (odds ratio for highest versus lowest quintile, 0.37; 95% CI 0.18-0.76) and by low SOAT1 (zeige SOAT1 Proteine) expression (odds ratio, 0.41; 95% CI 0.21-0.83).
LDLR associated with Familial Hypercholesterolemia and Polygenic Hypercholesterolemia in patients with Acute Coronary Syndrome , age =65 years, and LDL-C levels >/=160 mg/dl.
Chinese W483X mutation in the low-density lipoprotein-receptor gene in young patients with homozygous familial hypercholesterolemia
Proprotein convertase subtilisin (zeige PCSK9 Proteine)/kexin 9 V4I variant with LDLR mutations modifies the phenotype of familial hypercholesterolemia
both LDLR rs6511720 and rs57217136 are functional variants; both these minor alleles create enhancer-binding protein sites for transcription factors and may contribute to increased LDLR expression, which is consequently associated with reduced LDL-C levels and 12% lower coronary heart disease risk
Using assays that measured conformational change, acid-dependent lipoprotein release, LDLR recycling, and net lipoprotein uptake, we show that H635 plays important roles in acid-dependent conformational change and lipoprotein release, while H264, H306, and H439 play ancillary roles in the response of the LDLR to acidic pH
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.
Cdkn2a transcripts modulate platelet production and activity in the setting of hypercholesterolemic LDLR knockout mice.
Lysosomal oxLDL accumulation within macrophages contributes to murine atherosclerosis. Prevention of oxLDL uptake leads to decreased atherosclerosis in hematopoietic NPC1 (zeige NPC1 Proteine)-deficient Ldlr(-/-) mice
CD11b (zeige ITGAM Proteine)+Gr-1 (zeige GSR Proteine)+ myeloid-derived suppressor cells suppress T cells in an IFN-gamma (zeige IFNG Proteine)- and nitric oxide-dependent manner to reduce atherosclerotic lesion development in LDLr deficient mice.
This study investigated the effects of Aerobic exercise training on endothelial dysfunction and vascular redox status in the aortas of LDL receptor knockout mice (LDLr(-/-)), a genetic model of familial hypercholesterolemia.
PTP1B (zeige PTPN1 Proteine) inhibitors protect against atherosclerotic plaque formation in the LDLR(-/-) mouse model of atherosclerosis.
ApoC-III (zeige APOC3 Proteine) inhibits turnover of TG-rich lipoproteins primarily through a hepatic clearance mechanism mediated by the LDLR/LRP1 (zeige LRP1 Proteine) axis
Leukocyte GPR120/FFAR4 WT or KO mice in the LDL receptor KO background were generated by bone marrow transplantation.leukocyte GPR120 expression has minimal effects on dietary PUFA-induced plasma lipid/lipoprotein reduction and atheroprotection, and there is no distinction between n-3 versus n-6 PUFAs in activating anti-inflammatory effects of leukocyte GPR120/FFAR4 in vivo
This study reports the creation of a mouse model of autoimmunity-associated atherosclerosis by transplanting bone marrow from FcgammaRIIB knockout (FcRIIB(-/-)) mice into LDL receptor knockout 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 (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)