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Lipoproteins, LDLLipoproteinsReceptors, LDLReceptors, LipoproteinLipoproteins, HDLLipoproteins, VLDLLipoprotein LipaseLipoprotein(a)CholesterolCholesterol, LDLHyperlipoproteinemia Type IIApolipoproteins BApolipoproteins ELow Density Lipoprotein Receptor-Related Protein-1TriglyceridesApolipoproteinsLDL-Receptor Related ProteinsLipoproteins, IDLLipidsLipoproteins, HDL3Cholesterol EstersCholesterol, HDLScavenger Receptors, Class EHypercholesterolemiaApolipoprotein B-100LiverProprotein ConvertasesScavenger Receptors, Class BHyperlipidemiasArteriosclerosisHydroxymethylglutaryl CoA ReductasesChylomicronsReceptors, ScavengerCholesterol, DietaryLipoproteins, HDL2AtherosclerosisHeymann Nephritis Antigenic ComplexLDL-Receptor Related Protein-Associated ProteinReceptors, Oxidized LDLLipid MetabolismAntigens, CD36Receptors, Cell SurfaceSerine EndopeptidasesCholesterol, VLDLApolipoproteins ACells, CulturedSterolsMolecular Sequence DataApolipoprotein E3KineticsApolipoproteins CCricetinaeMice, KnockoutLipaseEndocytosisFoam CellsReceptors, ImmunologicMacrophagesApolipoprotein E2RNA, MessengerProtein BindingLovastatinAmino Acid SequenceHypertriglyceridemiaAnticholesteremic AgentsMice, Inbred C57BLSterol O-AcyltransferaseSterol Regulatory Element Binding Protein 2Diet, AtherogenicFibroblastsHydroxycholesterolsBase SequenceUltracentrifugationCell LineAortaCHO CellsRabbitsCarrier ProteinsEthinyl EstradiolDietary FatsCell Adhesion Molecules, NeuronalApolipoprotein C-IIIOxidation-ReductionCholesterol Ester Transfer ProteinsPhospholipidsMutationHomozygoteCell MembraneRhinovirusEsterificationApolipoprotein C-IApolipoprotein B-48Particle SizeElectrophoresis, Polyacrylamide GelHyperlipoproteinemia Type IIIIodine RadioisotopesHyperlipoproteinemiasProbucolHydroxymethylglutaryl-CoA Reductase InhibitorsBiological Transport
VLDLLDLRTriglyceride-rich lipoproteinsProteinEndocytosisScavenger receptorsDensity lipoproteinUptakeClathrin-coated pitsApoERepeatsCholesterol metabolismFamilial hypercholesterolemiaParticlesGeneAtherosclerosisAtherogenesisConcentrationsYWTDExtracellular matrixLiver X receptTLR4ResiduesHypertriglyceridemiaBoundOccurMutationsLipidDegradationTransportersSignificantlyDramaticallySpecificExpressionDomainsClassCellFound
VLDL9
  • It is a cell-surface receptor that recognizes apolipoprotein B100 (ApoB100), which is embedded in the outer phospholipid layer of very low-density lipoprotein (VLDL), their remnants-i.e. intermediate-density lipoprotein (IDL), and LDL particles. (wikipedia.org)
  • VLDL = very low-density lipoprotein. (medscape.com)
  • LDL is formed from very low-density lipoprotein (VLDL) and is catabolized predominantly by the high affinity LDL receptor. (nih.gov)
  • The mechanism of the LDL-lowering effect of lovastatin may involve both reduction of VLDL-C concentration, and induction of the LDL receptor, leading to reduced production and/or increased catabolism of LDL-C. Apolipoprotein B also falls during treatment with lovastatin. (nih.gov)
  • Rosuvastatin also inhibits hepatic synthesis of very low-density lipoprotein (VLDL). (pediatriconcall.com)
  • The overall effect is a decrease in plasma LDL and VLDL. (pediatriconcall.com)
  • As apoE2 binds defectively to LDL receptors, apoE2 homozygosity can precipitate type III hyperlipoproteinemia, however, only occurs when another condition, including: diabetes, oestrogen deficiency, hypothyroidism, or obesity, leads to the overproduction of VLDL or fewer LDL receptors, overwhelming the limited ability of apoE2 to mediate the clearance of triglyceride-rich and cholesterol-rich β-VLDL. (randox.com)
  • The lipoprotein-binding preference of apoE4 to large (30-80nm), triglyceride-rick VLDL, is associated with elevated levels of LDL. (randox.com)
  • The enrichment of VLDL with apoE4 accelerates their clearance from the plasma by receptor-mediated endocytosis in the liver and consequently, LDL receptors are downregulated, and LDL levels rise 3 . (randox.com)
LDLR7
  • In humans, the LDL receptor protein is encoded by the LDLR gene on chromosome 19. (wikipedia.org)
  • Individuals with disruptive mutations (defined as nonsense, splice site, or indel frameshift) in LDLR have an average LDL-cholesterol of 279 mg/dL, compared with 135 mg/dL for individuals with neither disruptive nor deleterious mutations. (wikipedia.org)
  • This protein belongs to the LDLR family and is made up of a number of functionally distinct domains, including 3 EGF-like domains, 7 LDL-R class A domains, and 6 LDL-R class B repeats. (wikipedia.org)
  • These modules include a putative signal peptide for protein export, four epidermal growth factor (EGF) repeats with associated spacer domains, three LDL-receptor (LDLR) repeats, a single transmembrane spanning domain, and a cytoplasmic domain. (nih.gov)
  • Ng lipoproteins are taken up by two functionally significant low-density lipoprotein (LDL) receptors: the prototypic LDL receptor (LDLR) along with the LDL receptor-related protein 1 (LRP1). (nicotinic-receptor.com)
  • The low-density lipoprotein receptor (LDLR) is the major cholesterol-carrying lipoprotein of plasma, acting to regulate cholesterol homeostasis in mammalian cells. (embl.de)
  • Residual remnant lipoproteins can be taken up via LRP1 or even LDLR or VLDLR. (jci.org)
Triglyceride-rich lipoproteins2
Protein7
  • The low-density lipoprotein receptor (LDL-R) is a mosaic protein of 839 amino acids (after removal of 21-amino acid signal peptide) that mediates the endocytosis of cholesterol-rich low-density lipoprotein (LDL). (wikipedia.org)
  • e.g. a truncation of the receptor protein at residue number 660 leads to domains 3,4 and 5 of the EGF precursor domain being missing. (wikipedia.org)
  • This precludes the movement of the receptor from the ER to the Golgi, and leads to degradation of the receptor protein. (wikipedia.org)
  • The gene, termed low-density lipoprotein receptor related protein 5 (LRP5), encodes a protein of 1615 amino acids that contains conserved modules which are characteristic of the low-density lipoprotein (LDL) receptor family. (nih.gov)
  • Other homologous domains occur in related receptors, including the very low-density lipoprotein receptor and the LDL receptor-related protein/alpha 2-macroglobulin receptor, and in proteins which are functionally unrelated, such as the C9 component of complement. (embl.de)
  • LDL/IgG complexes can be internalized via Fc receptors, and lipoproteins bound by IgM or C-reactive protein (CRP) can in turn bind complement and undergo enhanced binding via complement receptors. (jci.org)
  • The apoE protein binds with lipid forming lipoproteins which are responsible for the transportation of cholesterol and other lipids through the bloodstream 1 . (randox.com)
Endocytosis3
  • The cytosolic C-terminal domain contains ~50 amino acids, including a signal sequence important for localizing the receptors to clathrin-coated pits and for triggering receptor-mediated endocytosis after binding. (wikipedia.org)
  • Following receptor-mediated endocytosis, ApoE is recycled for the plasma membrane, and cholesterol is used for cell membrane turnover and repair, myelin formation, synaptogenesis and neurotransmitter release [146]. (nicotinic-receptor.com)
  • The LDL receptor binds LDL and transports it into cells by acidic endocytosis. (embl.de)
Scavenger receptors4
  • TLR4), and scavenger receptors involved in cholesterol uptake (SR-AI, CD-36). (biorxiv.org)
  • 2007) by attenuating the expression of scavenger receptors (SRS) and lectin-like oxidized low-density lipoproteins (ox-LDL). (scialert.net)
  • Macrophage scavenger receptors, such as CD36 and class A scavenger receptor (SR-A), have previously been thought to play a central role in foam cell formation and atherogenesis by mediating the uptake of oxidized LDL. (jci.org)
  • Scavenger receptors expressed on the surface of macrophages that may contribute to the uptake of modified lipoproteins include SR-A, CD36, SR-BI, PSOX, MARCO, and lectin-like OxLDL receptor 1 (LOX-1). (jci.org)
Density lipoprotein13
  • It belongs to the low density lipoprotein receptor gene family. (wikipedia.org)
  • Hyperlipidemia comprises a heterogeneous group of disorders, characterized by high levels in one or more lipids and/or lipoproteins [atherogenic free fatty acids (FA), triglycerides (TG) (hypertriglyceridemia), small dense low-density lipoprotein cholesterol (LDL-C) (hypercholesterolemia), and apolipoprotein (apo) B], and/or low level in antiatherogenic high density lipoprotein cholesterol (HDL-C), in the circulation [ 1 - 3 ]. (hindawi.com)
  • The present study aimed to investigate the effects of S/V on the expression of metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1), inflammation and apoptosis in human umbilical vein endothelial cells (HUVECs) induced by oxidized low‑density lipoprotein (ox‑LDL) and to elucidate its possible mechanism. (spandidos-publications.com)
  • Oxidized low-density lipoprotein (ox-LDL) is widely recognized to participate in the occurrence and development of atherosclerosis through inducing oxidative chain reaction and endothelial dysfunction ( 6 ). (spandidos-publications.com)
  • The involvement of low-density lipoprotein cholesterol (LDL-C) in atherogenesis has been well-documented in clinical and pathological studies, as well as in many animal experiments. (nih.gov)
  • Epidemiological and clinical studies have established that high LDL-C and low high-density lipoprotein cholesterol (HDL-C) are both associated with coronary heart disease. (nih.gov)
  • Cysteine-rich repeat in the low-density lipoprotein (LDL) receptor that plays a central role in mammalian cholesterol metabolism. (embl.de)
  • Decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low-density lipoprotein (LDL) receptors which increases hepatic uptake of LDL. (pediatriconcall.com)
  • The repeat is found in a variety of proteins that include, vitellogenin receptor from Drosophila melanogaster, low-density lipoprotein (LDL) receptor [ ( PUBMED:6091915 ) ], preproepidermal growth factor, and nidogen (entactin). (embl.de)
  • Complete cloning and sequencing of rat gp330/"megalin," a distinctive member of the low density lipoprotein receptor gene family. (embl.de)
  • Familial hypercholesterolemia (FH) is an autosomal dominant disorder that causes severe elevations in total cholesterol and low-density lipoprotein cholesterol (LDLc). (medscape.com)
  • Using data from the second phase (1991-1994) of the Third National Health and Nutrition Examination Survey (NHANES III), we examined associations between 22 polymorphisms in 13 candidate genes and four serum lipids: high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and triglycerides (TG). (cdc.gov)
  • Previous reports from the Framingham Heart Study suggested a strong positive relationship between coronary heart disease and elevated levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels, in addition to an inverse relationship between the disease and high-density lipoprotein cholesterol (HDL-C) levels [ 5 - 8 ]. (cdc.gov)
Uptake3
  • TZDs markedly stimulate the uptake of oxidized LDL (oxLDL) into adipocytes, and this requires OLR1. (jci.org)
  • Thus, the HSP27 IC potentiates HSP27 cell membrane signaling with receptors involved in modulating inflammation and cholesterol uptake, as well as HSP27 internalization. (biorxiv.org)
  • Finally, uptake of native, modified or aggregated LDL could occur via stimulated macropinocytosis, independent of or in association with receptor-mediated uptake. (jci.org)
Clathrin-coated pits2
  • In order to be internalized, the receptor-ligand complex must first cluster into clathrin-coated pits. (embl.de)
  • The fifth domain is the cytoplasmic tail that directs the receptor to clathrin-coated pits. (embl.de)
ApoE4
  • The receptor also recognizes apolipoprotein E (ApoE) which is found in chylomicron remnants and IDL. (wikipedia.org)
  • The key function of apoE is to mediate the binding of lipoproteins or lipid complexes in the plasma or interstitial fluids to specific cell-surface receptors. (randox.com)
  • These receptors internalise apoE-containing lipoprotein particles and so apoE participates in the distribution or redistribution of lipids among various tissues and bodily cells. (randox.com)
  • Other dominant and recessive mutations in apoE that affect residues in or around the receptor binding region also causes type III hyperlipoproteinemia 3 . (randox.com)
Repeats3
  • The N-terminal domain of the LDL receptor, which is responsible for ligand binding, is composed of seven sequence repeats (~50% identical). (wikipedia.org)
  • The exact mechanism of interaction between the class A repeats and ligand (LDL) is unknown, but it is thought that the repeats act as "grabbers" to hold the LDL. (wikipedia.org)
  • The N-terminal type A repeats in LDL receptor bind the lipoproteins. (embl.de)
Cholesterol metabolism1
  • Michael S. Brown and Joseph L. Goldstein were awarded the 1985 Nobel Prize in Physiology or Medicine for their identification of LDL-R and its relation to cholesterol metabolism and familial hypercholesterolemia. (wikipedia.org)
Familial hypercholesterolemia1
Particles1
  • Hyperlipoproteinemia is a metabolic disorder characterized by abnormally elevated concentrations of specific lipoprotein particles in the plasma. (medscape.com)
Gene3
  • Mutations in the gene encoding the LDL receptor are known to cause familial hypercholesterolaemia. (wikipedia.org)
  • Here we report that antidiabetic thiazolidinediones (TZDs) and other ligands for the nuclear receptor PPARγ dramatically upregulate oxidized LDL receptor 1 (OLR1) in adipocytes by facilitating the exchange of coactivators for corepressors on the OLR1 gene in cultured mouse adipocytes. (jci.org)
  • Definitive diagnosis can be made only with gene or receptor analysis. (medscape.com)
Atherosclerosis4
Atherogenesis2
  • In contrast, similar studies by previous investigators found that deletion of these receptors decreased atherogenesis. (jci.org)
  • The reasons for the different results are not known, but these data suggest that the role of these receptors in atherogenesis remains unresolved. (jci.org)
Concentrations2
  • Lovastatin has been shown to reduce elevated LDL-C concentrations. (nih.gov)
  • Results from our study contribute to a growing body of literature identifying key determinants of plasma lipoprotein concentrations and could provide insight into the biological mechanisms underlying serum lipid and cholesterol concentrations. (cdc.gov)
YWTD1
  • A, B and C. A and B are closely linked while C is separated by the YWTD repeat region, which adopts a beta-propeller conformation (LDL-R class B domain). (wikipedia.org)
Extracellular matrix1
  • It has been speculated that the domain may have ancestrally acted as a spacer to push the receptor beyond the extracellular matrix. (wikipedia.org)
Liver X recept2
  • The nuclear hormone receptors liver X receptor α (LXRα) and LXRβ function as physiological receptors for oxidized cholesterol metabolites (oxysterols) and regulate several aspects of cholesterol and lipid metabolism. (aspetjournals.org)
  • Transcription of these transporters is regulated by PPARγ and liver X receptor (LXR), and they are also subject to posttranscriptional regulation by apoAI. (jci.org)
TLR43
  • A nitric oxide (NO) detection kit was used to determine the concentration of NO. Western blotting analysis was performed to determine the levels of intercellular cell adhesion molecule (ICAM)‑1, vascular cell adhesion molecule (VCAM)‑1, endothelin‑1, caspase‑3, Bax, Bcl‑2, Toll‑like receptor 4 (TLR4), p65 and p‑p65. (spandidos-publications.com)
  • Compared with the ox‑LDL group, S/V treatment significantly increased the cell viability, NO concentration and Bcl‑2 expression, decreased the levels of IL‑1β, IL‑6 and TNF‑α and reduced the expressions of MALAT1, ICAM‑1, VCAM‑1, cleaved‑caspase‑3, Bax, TLR4 and p‑p65. (spandidos-publications.com)
  • Overall, the findings suggested that S/V could downregulate the expression of MALAT1, inhibit inflammation and apoptosis and improve endothelial function in ox‑LDL‑induced HUVECs via inactivating the TLR4/NF‑κB signaling pathway. (spandidos-publications.com)
Residues2
  • Each repeat, referred to as a class A repeat or LDL-A, contains roughly 40 amino acids, including 6 cysteine residues that form disulfide bonds within the repeat. (wikipedia.org)
  • Numerous familial hypercholestorolemia mutations of the LDL receptor alter the calcium coordinating residue of LDL-A domains or other crucial scaffolding residues. (embl.de)
Hypertriglyceridemia1
Bound1
  • It is thought that this region is responsible for the pH-dependent conformational shift that causes bound LDL to be released in the endosome. (wikipedia.org)
Occur1
  • However, the risk of developing coronary heart disease is continuous and graded over the range of cholesterol levels and many coronary events do occur in patients with total cholesterol (total-C) and LDL-C in the lower end of this range. (nih.gov)
Mutations2
  • There are 5 broad classes of mutation of the LDL receptor: Class 1 mutations affect the synthesis of the receptor in the endoplasmic reticulum (ER). (wikipedia.org)
  • Class 2 mutations prevent proper transport to the Golgi body needed for modifications to the receptor. (wikipedia.org)
Lipid1
  • The genetic basis for elevation in lipid levels is not well understood, but substantial heritability has been demonstrated in twin [ 9 ] and family-based [ 10 - 12 ] studies, which have estimated that approximately 43% to 83% of the variance in blood lipid and lipoprotein levels is attributable to genetic factors. (cdc.gov)
Degradation1
  • Phagocytosis is a term coined from the Greek to describe the receptor-mediated engulfment and degradation of dead cells and microbes. (frontiersin.org)
Transporters1
  • Different transporters and receptors present at the BBB have been described as playing roles in maintaining the integrity of the BBB and brain homeostasis. (aspetjournals.org)
Significantly1
  • However, the PON1 A-G haplotype was significantly associated with LDL-C and TC. (cdc.gov)
Dramatically1
  • Most patients with homozygous FH do not survive adulthood beyond age 30 years unless treated with unusual methods, such as liver transplantation, LDL apheresis, or ileal bypass surgery to dramatically lower their LDLc levels. (medscape.com)
Specific1
  • LDL receptor analysis can be used to identify the specific LDL receptor defect, and LDL receptor or apoB-100 studies can help distinguish heterozygous FH from the similar syndrome of familial defective apoB-100. (medscape.com)
Expression1
  • Previous studies have shown that the expression of MALAT1 is increased in endothelial cells induced by ox-LDL and its expression level can reflect the damage degree of endothelial cells ( 11 , 12 ). (spandidos-publications.com)
Domains1
  • In LDL receptors, the class A domains form the binding site for LDL and calcium. (embl.de)
Class1
  • Conversely, major histocompatibility complex class I polypeptide-related sequence A (MHC1A) (O.R.=0.6) and natural cytotoxicity triggering receptor 3 (NCR3) (O.R.=0.46) were associated with lower odds. (medrxiv.org)
Cell1
  • Exon 1 contains a signal sequence that localises the receptor to the endoplasmic reticulum for transport to the cell surface. (wikipedia.org)
Found1
  • Portions of the cytosolic sequence have been found in other lipoprotein receptors, as well as in more distant receptor relatives. (wikipedia.org)