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Human LDLR ELISA Kit for Sandwich ELISA - ABIN2345050
Alvarez, Khosroheidari, Eddy, Done: MicroRNA-27a decreases the level and efficiency of the LDL receptor and contributes to the dysregulation of cholesterol homeostasis. in Atherosclerosis 2015
Human LDLR ELISA Kit for Sandwich ELISA - ABIN414516
Su, Li, Liang, Qi: Synthetic low-density lipoprotein (sLDL) selectively delivers paclitaxel to tumor with low systemic toxicity. in Oncotarget 2016
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 ELISA Kits)-depleted culture medium at the same levels as unmodified liposomes in FBS (show FBXO8 ELISA Kits)-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 ELISA Kits) or LDLR (or both).
These findings suggest that LDLR rs2738464 may affect the affinity of miR-330 binding to the LDLR 3'-UTR, thus regulating LDLR expression and contributing to clear cell renal cell carcinoma 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 ELISA Kits)-overexpressing breast cancers in the setting of elevated circulating LDL cholesterol (LDL-C).
Identify LDLR, APOB (show APOB ELISA Kits) and PCSK9 (show PCSK9 ELISA Kits) 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 (show PCSK9 ELISA Kits) 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
Nonesterified fatty acids significantly inhibit the expression of ApoB100 (show APOB ELISA Kits), ApoE (show APOE ELISA Kits), MTP (show MTTP ELISA Kits), and LDLR, thereby decreasing the synthesis and assembly of VLDL and inducing TG accumulation in bovine hepatocytes.
both LRP1 (show LRP1 ELISA Kits) and LDLR expression and agLDL uptake are regulated by P2Y2R (show P2RY2 ELISA Kits) in vascular smooth muscle cells, and agLDL uptake due to P2Y2R (show P2RY2 ELISA Kits) activation is dependent upon cytoskeletal reorganization mediated by P2Y2R (show P2RY2 ELISA Kits) binding to FLN-A (show FLNA ELISA Kits)
this study shows that STAT4 (show STAT4 ELISA Kits) regulates the CD8 (show CD8A ELISA Kits)(+) regulatory T cell/T follicular helper cell axis and promotes atherogenesis in insulin (show INS ELISA Kits)-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 ELISA Kits) allele (E4 versus E3) and docosahexaenoic acid intake. (APOE (show APOE ELISA Kits) = apolipoprotein E (show APOE ELISA Kits))
increased blood pressure and reduced aortic compliance are not direct causes of increased aortic plaque accumulation in a model of LDLR knockout mice
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 (show NPC1 ELISA Kits)-deficient Ldlr(-/-) mice
CD11b (show ITGAM ELISA Kits)+Gr-1 (show GSR ELISA Kits)+ myeloid-derived suppressor cells suppress T cells in an IFN-gamma (show IFNG ELISA Kits)- 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.
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 ELISA Kits) and SREBP-Sp1 (show SP1 ELISA Kits) activation interact to regulate low density lipoprotein receptor promoter function
found association between genotypes for LDLR and APOB (show APOB ELISA Kits) 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)