Apolipoproteins B: Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.Apolipoprotein A-I: The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.Apolipoprotein B-100: A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.Apolipoprotein B-48: A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.Apolipoproteins E: A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.Apolipoproteins: Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.Apolipoprotein C-III: A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).Apolipoproteins A: Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.Apolipoprotein E4: A major and the second most common isoform of apolipoprotein E. In humans, Apo E4 differs from APOLIPOPROTEIN E3 at only one residue 112 (cysteine is replaced by arginine), and exhibits a lower resistance to denaturation and greater propensity to form folded intermediates. Apo E4 is a risk factor for ALZHEIMER DISEASE and CARDIOVASCULAR DISEASES.Apolipoprotein E3: A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.Lipoproteins, VLDL: A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.Apolipoprotein A-II: The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.Lipoproteins: Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.Apolipoprotein C-II: A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.Lipoproteins, LDL: A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.TriglyceridesCholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Apolipoprotein E2: One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.Apolipoprotein C-I: A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.Apolipoproteins C: A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.Lipoproteins, HDL: A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.Lipids: A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)Hypobetalipoproteinemias: Conditions with abnormally low levels of BETA-LIPOPROTEINS (low density lipoproteins or LDL) in the blood. It is defined as LDL values equal to or less than the 5th percentile for the population. They include the autosomal dominant form involving mutation of the APOLIPOPROTEINS B gene, and the autosomal recessive form involving mutation of the microsomal triglyceride transfer protein. All are characterized by low LDL and dietary fat malabsorption.Apoprotein(a): A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.Cholesterol, LDL: Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.Lipoprotein(a): A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.Cytidine Deaminase: An enzyme that catalyzes the deamination of cytidine, forming uridine. EC 3.5.4.5.Receptors, LDL: Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.RNA Editing: A process that changes the nucleotide sequence of mRNA from that of the DNA template encoding it. Some major classes of RNA editing are as follows: 1, the conversion of cytosine to uracil in mRNA; 2, the addition of variable number of guanines at pre-determined sites; and 3, the addition and deletion of uracils, templated by guide-RNAs (RNA, GUIDE).Cholesterol, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.Lipoproteins, IDL: A mixture of very-low-density lipoproteins (VLDL), particularly the triglyceride-poor VLDL, with slow diffuse electrophoretic mobilities in the beta and alpha2 regions which are similar to that of beta-lipoproteins (LDL) or alpha-lipoproteins (HDL). They can be intermediate (remnant) lipoproteins in the de-lipidation process, or remnants of mutant CHYLOMICRONS and VERY-LOW-DENSITY LIPOPROTEINS which cannot be metabolized completely as seen in FAMILIAL DYSBETALIPOPROTEINEMIA.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Hyperlipidemia, Familial Combined: A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.Hyperlipoproteinemia Type II: A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).Hyperlipidemias: Conditions with excess LIPIDS in the blood.Hypobetalipoproteinemia, Familial, Apolipoprotein B: An autosomal dominant disorder of lipid metabolism. It is caused by mutations of APOLIPOPROTEINS B, main components of CHYLOMICRONS and BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include abnormally low LDL, normal triglyceride level, and dietary fat malabsorption.Hypolipoproteinemias: Conditions with abnormally low levels of LIPOPROTEINS in the blood. This may involve any of the lipoprotein subclasses, including ALPHA-LIPOPROTEINS (high-density lipoproteins); BETA-LIPOPROTEINS (low-density lipoproteins); and PREBETA-LIPOPROTEINS (very-low-density lipoproteins).Chylomicrons: A class of lipoproteins that carry dietary CHOLESTEROL and TRIGLYCERIDES from the SMALL INTESTINE to the tissues. Their density (0.93-1.006 g/ml) is the same as that of VERY-LOW-DENSITY LIPOPROTEINS.Arteriosclerosis: Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.Lipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Hyperlipoproteinemias: Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.Apolipoproteins D: A glycoprotein component of HIGH-DENSITY LIPOPROTEINS that transports small hydrophobic ligands including CHOLESTEROL and STEROLS. It occurs in the macromolecular complex with LECITHIN CHOLESTEROL ACYLTRANSFERASE. Apo D is expressed in and secreted from a variety of tissues such as liver, placenta, brain tissue and others.Hypercholesterolemia: A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.Oleic Acid: An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed)Abetalipoproteinemia: An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.Cholesterol, VLDL: Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Hyperlipoproteinemia Type IV: A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits.Hypertriglyceridemia: A condition of elevated levels of TRIGLYCERIDES in the blood.Lipoprotein Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Alleles: Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.Receptors, Lipoprotein: Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.Phosphatidylcholine-Sterol O-Acyltransferase: An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.Hyperlipoproteinemia Type III: An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Mice, Inbred C57BLDietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.Anticholesteremic Agents: Substances used to lower plasma CHOLESTEROL levels.Polymorphism, Genetic: The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.Heterozygote: An individual having different alleles at one or more loci regarding a specific character.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Nephelometry and Turbidimetry: Chemical analysis based on the phenomenon whereby light, passing through a medium with dispersed particles of a different refractive index from that of the medium, is attenuated in intensity by scattering. In turbidimetry, the intensity of light transmitted through the medium, the unscattered light, is measured. In nephelometry, the intensity of the scattered light is measured, usually, but not necessarily, at right angles to the incident light beam.Cholesterol Ester Transfer Proteins: Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.Intestines: The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.Kinetics: The rate dynamics in chemical or physical systems.Methaqualone: A quinazoline derivative with hypnotic and sedative properties. It has been withdrawn from the market in many countries because of problems with abuse. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604)Cholesterol, Dietary: Cholesterol present in food, especially in animal products.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.ATP Binding Cassette Transporter 1: A superfamily of large integral ATP-binding cassette membrane proteins whose expression pattern is consistent with a role in lipid (cholesterol) efflux. It is implicated in TANGIER DISEASE characterized by accumulation of cholesteryl ester in various tissues.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Ultracentrifugation: Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Aorta: The main trunk of the systemic arteries.Homozygote: An individual in which both alleles at a given locus are identical.Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.Hypolipidemic Agents: Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Particle Size: Relating to the size of solids.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Triolein: (Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.Dyslipidemias: Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.Hydroxymethylglutaryl-CoA Reductase Inhibitors: Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.Reference Values: The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.Risk Factors: An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.Heptanoic Acids: 7-carbon saturated monocarboxylic acids.Endoplasmic Reticulum: A system of cisternae in the CYTOPLASM of many cells. In places the endoplasmic reticulum is continuous with the plasma membrane (CELL MEMBRANE) or outer membrane of the nuclear envelope. If the outer surfaces of the endoplasmic reticulum membranes are coated with ribosomes, the endoplasmic reticulum is said to be rough-surfaced (ENDOPLASMIC RETICULUM, ROUGH); otherwise it is said to be smooth-surfaced (ENDOPLASMIC RETICULUM, SMOOTH). (King & Stansfield, A Dictionary of Genetics, 4th ed)Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Oleic Acids: A group of fatty acids that contain 18 carbon atoms and a double bond at the omega 9 carbon.Coronary Disease: An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.Sterol O-Acyltransferase: An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.Diet, Atherogenic: A diet that contributes to the development and acceleration of ATHEROGENESIS.Hepatocytes: The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.Postprandial Period: The time frame after a meal or FOOD INTAKE.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Clusterin: A highly conserved heterodimeric glycoprotein that is differentially expressed during many severe physiological disturbance states such as CANCER; APOPTOSIS; and various NEUROLOGICAL DISORDERS. Clusterin is ubiquitously expressed and appears to function as a secreted MOLECULAR CHAPERONE.Cytidine: A pyrimidine nucleoside that is composed of the base CYTOSINE linked to the five-carbon sugar D-RIBOSE.Pedigree: The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.Leupeptins: A group of acylated oligopeptides produced by Actinomycetes that function as protease inhibitors. They have been known to inhibit to varying degrees trypsin, plasmin, KALLIKREINS, papain and the cathepsins.Biological Transport: The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.Alzheimer Disease: A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)Time Factors: Elements of limited time intervals, contributing to particular results or situations.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Colestipol: Highly crosslinked and insoluble basic anion exchange resin used as anticholesteremic. It may also may reduce triglyceride levels.Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.Tumor Cells, Cultured: Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.Immunoassay: A technique using antibodies for identifying or quantifying a substance. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance.Kringles: Triple-looped protein domains linked by disulfide bonds. These common structural domains, so-named for their resemblance to Danish pastries known as kringlers, play a role in binding membranes, proteins, and phospholipids as well as in regulating proteolysis. Kringles are also present in coagulation-related and fibrinolytic proteins and other plasma proteinases.Gene Frequency: The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.Radioimmunoassay: Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.Macrophages: The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Fasting: Abstaining from all food.Egg Proteins, Dietary: Proteins found in eggs which are consumed as a food.DNA: A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).Polymorphism, Restriction Fragment Length: Variation occurring within a species in the presence or length of DNA fragment generated by a specific endonuclease at a specific site in the genome. Such variations are generated by mutations that create or abolish recognition sites for these enzymes or change the length of the fragment.Proprotein Convertases: Proteolytic enzymes that are involved in the conversion of protein precursors such as peptide prohormones into PEPTIDE HORMONES. Some are ENDOPEPTIDASES, some are EXOPEPTIDASES.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Fatty Acids: Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)Tangier Disease: An autosomal recessively inherited disorder caused by mutation of ATP-BINDING CASSETTE TRANSPORTERS involved in cellular cholesterol removal (reverse-cholesterol transport). It is characterized by near absence of ALPHA-LIPOPROTEINS (high-density lipoproteins) in blood. The massive tissue deposition of cholesterol esters results in HEPATOMEGALY; SPLENOMEGALY; RETINITIS PIGMENTOSA; large orange tonsils; and often sensory POLYNEUROPATHY. The disorder was first found among inhabitants of Tangier Island in the Chesapeake Bay, MD.Triazenes: Compounds with three contiguous nitrogen atoms in linear format, H2N-N=NH, and hydrocarbyl derivatives.Sulfur Radioisotopes: Unstable isotopes of sulfur that decay or disintegrate spontaneously emitting radiation. S 29-31, 35, 37, and 38 are radioactive sulfur isotopes.Carcinoma, Hepatocellular: A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Phosphatidylcholines: Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a choline moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and choline and 2 moles of fatty acids.1-Propanol: A colorless liquid made by oxidation of aliphatic hydrocarbons that is used as a solvent and chemical intermediate.Electrophoresis, Agar Gel: Electrophoresis in which agar or agarose gel is used as the diffusion medium.Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Lymph: The interstitial fluid that is in the LYMPHATIC SYSTEM.Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.Pyrroles: Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.Lipolysis: The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.ATP-Binding Cassette Transporters: A family of MEMBRANE TRANSPORT PROTEINS that require ATP hydrolysis for the transport of substrates across membranes. The protein family derives its name from the ATP-binding domain found on the protein.DNA Primers: Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.High-Density Lipoproteins, Pre-beta: A highly dense subclass of the high-density lipoproteins, with particle sizes below 7 nm. They are also known as nascent HDL, composed of a few APOLIPOPROTEIN A-I molecules which are complexed with PHOSPHOLIPIDS. The lipid-poor pre-beta-HDL particles serve as progenitors of HDL3 and then HDL2 after absorption of free cholesterol from cell membranes, cholesterol esterification, and acquisition of apolipoproteins A-II, Cs, and E. Pre-beta-HDL initiate the reverse cholesterol transport process from cells to liver.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Dimyristoylphosphatidylcholine: A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.Fenofibrate: An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.RNA Processing, Post-Transcriptional: Post-transcriptional biological modification of messenger, transfer, or ribosomal RNAs or their precursors. It includes cleavage, methylation, thiolation, isopentenylation, pseudouridine formation, conformational changes, and association with ribosomal protein.AzetidinesOxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).Fatty Acids, Monounsaturated: Fatty acids which are unsaturated in only one position.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.FluorobenzenesImmunosorbent Techniques: Techniques for removal by adsorption and subsequent elution of a specific antibody or antigen using an immunosorbent containing the homologous antigen or antibody.Strikes, Employee: Work-related situations in which the employees as a group refuse to work until certain conditions of employment are granted by the employer.Cross-Over Studies: Studies comparing two or more treatments or interventions in which the subjects or patients, upon completion of the course of one treatment, are switched to another. In the case of two treatments, A and B, half the subjects are randomly allocated to receive these in the order A, B and half to receive them in the order B, A. A criticism of this design is that effects of the first treatment may carry over into the period when the second is given. (Last, A Dictionary of Epidemiology, 2d ed)Chylomicron Remnants: Metabolic products of chylomicron particles in which TRIGLYCERIDES have been selectively removed by the LIPOPROTEIN LIPASE. These remnants carry dietary lipids in the blood and are cholesterol-rich. Their interactions with MACROPHAGES; ENDOTHELIAL CELLS; and SMOOTH MUSCLE CELLS in the artery wall can lead to ATHEROSCLEROSIS.Aortic Diseases: Pathological processes involving any part of the AORTA.Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.Lipoproteins, HDL3: Intermediate-density subclass of the high-density lipoproteins, with particle sizes between 7 to 8 nm. As the larger lighter HDL2 lipoprotein, HDL3 lipoprotein is lipid-rich.Hydroxymethylglutaryl CoA Reductases: Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.Microscopy, Electron: Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.Binding, Competitive: The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.Cardiovascular Diseases: Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.Isoelectric Focusing: Electrophoresis in which a pH gradient is established in a gel medium and proteins migrate until they reach the site (or focus) at which the pH is equal to their isoelectric point.Genetic Variation: Genotypic differences observed among individuals in a population.Intestine, Small: The portion of the GASTROINTESTINAL TRACT between the PYLORUS of the STOMACH and the ILEOCECAL VALVE of the LARGE INTESTINE. It is divisible into three portions: the DUODENUM, the JEJUNUM, and the ILEUM.Chemical Precipitation: The formation of a solid in a solution as a result of a chemical reaction or the aggregation of soluble substances into complexes large enough to fall out of solution.Epitopes: Sites on an antigen that interact with specific antibodies.Low Density Lipoprotein Receptor-Related Protein-1: A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.Foam Cells: Lipid-laden macrophages originating from monocytes or from smooth muscle cells.Models, Biological: Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.Diet: Regular course of eating and drinking adopted by a person or animal.Molecular Weight: The sum of the weight of all the atoms in a molecule.Niacin: A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.Microsomes: Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).Radioisotope Dilution Technique: Method for assessing flow through a system by injection of a known quantity of radionuclide into the system and monitoring its concentration over time at a specific point in the system. (From Dorland, 28th ed)Liver Neoplasms: Tumors or cancer of the LIVER.Restriction Mapping: Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.Coronary Artery Disease: Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.Diet, Fat-Restricted: A diet that contains limited amounts of fat with less than 30% of calories from all fats and less than 10% from saturated fat. Such a diet is used in control of HYPERLIPIDEMIAS. (From Bondy et al, Metabolic Control and Disease, 8th ed, pp468-70; Dorland, 27th ed)American Native Continental Ancestry Group: Individuals whose ancestral origins are in the continents of the Americas.LDL-Receptor Related Proteins: A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).Iodine Radioisotopes: Unstable isotopes of iodine that decay or disintegrate emitting radiation. I atoms with atomic weights 117-139, except I 127, are radioactive iodine isotopes.Cloning, Molecular: The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Diabetes Mellitus, Type 2: A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.Circular Dichroism: A change from planar to elliptic polarization when an initially plane-polarized light wave traverses an optically active medium. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Immunoblotting: Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.Transcription, Genetic: The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.Golgi Apparatus: A stack of flattened vesicles that functions in posttranslational processing and sorting of proteins, receiving them from the rough ENDOPLASMIC RETICULUM and directing them to secretory vesicles, LYSOSOMES, or the CELL MEMBRANE. The movement of proteins takes place by transfer vesicles that bud off from the rough endoplasmic reticulum or Golgi apparatus and fuse with the Golgi, lysosomes or cell membrane. (From Glick, Glossary of Biochemistry and Molecular Biology, 1990)Insulin: A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Rats, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Amyloidosis, Familial: Diseases in which there is a familial pattern of AMYLOIDOSIS.

Dietary fish oils inhibit early events in the assembly of very low density lipoproteins and target apoB for degradation within the rough endoplasmic reticulum of hamster hepatocytes. (1/731)

Dietary fish oils inhibited secretion and stimulated intracellular degradation of apolipoprotein (apo)B in hamster hepatocytes, while dietary sunflower oils stimulated secretion and had no effect on degradation of apoB. To investigate the intracellular site at which fish oils act, we have made use of our previous observations that inhibition of degradation by N-acetyl-leucyl-leucyl-norleucinal (ALLN) results in accumulation of apoB in the trans -Golgi membrane and does not stimulate secretion, while inhibition of degradation by o-phenanthroline results in accumulation of apoB in the rough endoplasmic reticulum membrane and stimulates secretion. Thus, ALLN protects apoB which has been diverted from secretion and o -phenanthroline protects apoB which is targetted for secretion. Addition of o -phenantholine to the incubation medium of hepatocytes from fish oil-fed hamsters inhibited degradation of apoB and stimulated its secretion in particles of the density of VLDL, while addition of ALLN had no effect. These observations suggest that dietary fish oils reversibly inhibit early steps in the assembly of very low density lipoprotein precursors and target apoB for degradation in the rough endoplasmic reticulum.  (+info)

Role of cholesterol ester mass in regulation of secretion of ApoB100 lipoprotein particles by hamster hepatocytes and effects of statins on that relationship. (2/731)

Our understanding of the factors that regulate the secretion of apoB100 lipoproteins remains incomplete with considerable debate as to the role, if any, for cholesterol ester in this process. This study examines this issue in primary cultures of hamster hepatocytes, a species in which both cholesterol and apoB100 metabolism are very similar to man. Addition of oleate to medium increased the mass of triglyceride and cholesterol ester within the hepatocyte and also increased the secretion of triglycerides, cholesterol ester, and apoB100 into the medium. Next, the responses of hamster hepatocytes to addition of either an HMG-CoA reductase inhibitor (lovastatin) or an acyl-CoA cholesterol acyltransferase inhibitor (58-035) to the medium, with or without added oleate, were determined. Effects of either agent were only evident in the oleate-supplemented medium in which cholesterol ester mass had been increased above basal. If oleate was not added to the medium, neither agent reduced apoB100 secretion; equally important, over the 24-hour incubation, neither agent, at the concentration used, produced any detectable change in intracellular cholesterol ester mass. However, in contrast to the estimates of mass, which were unchanged, under the same conditions radioisotopic estimates of cholesterol ester synthesis were markedly reduced. Any conclusion as to the relation of cholesterol ester mass to apoB100 secretion would therefore depend on which of the 2 methods was used. Overall, the data indicate a close correlation between the mass of cholesterol ester within the hepatocyte and apoB100 secretion from it and they go far to explain previous apparently contradictory data as to this relation. More importantly, though, taken with other available data, they indicate that the primary response of the liver to increased delivery of lipid is increased secretion rather than decreased uptake. These results point, therefore, to a hierarchy of hepatic responses to increased flux of fatty acids and increased synthesis of cholesterol that in turn suggests a more dynamic model of cholesterol homeostasis in the liver than has been appreciated in the past.  (+info)

Characterization of a new form of inherited hypercholesterolemia: familial recessive hypercholesterolemia. (3/731)

We previously described a Sardinian family in which the probands had a severe form of hypercholesterolemia, suggestive of familial hypercholesterolemia (FH). However, low density lipoprotein (LDL) receptor activity in fibroblasts from these subjects and LDL binding ability were normal. The characteristics of the pedigree were consistent with an autosomal recessive trait. Sitosterolemia and pseudohomozygous hyperlipidemia were ruled out. A second Sardinian kindred with similar characteristics was identified. Probands showed severe hypercholesterolemia, whereas their parents and grandparents were normolipidemic. FH, familial defective apoprotein (apo) B, sitosterolemia, and cholesteryl ester storage disease were excluded by in vitro studies. We addressed the metabolic basis of this inherited disorder by studying the in vivo metabolism of LDL in 3 probands from these 2 families. 125I-LDL turnover studies disclosed a marked reduction in the fractional catabolic rate (0.19+/-0.01 versus 0.36+/-0.03 pools per day, respectively; P<0.001) and a significant increase in the production rate [20.7+/-4.4 versus 14. 0+/-2.4 mg. kg-1. d-1, respectively; P<0.01] of LDL apoB in the probands compared with normolipidemic controls. We then studied the in vivo biodistribution and tissue uptake of 99mtechnetium-labeled LDL in the probands and compared them with those in normal controls and 1 FH homozygote. The probands showed a significant reduction in hepatic LDL uptake, similar to that observed in the FH homozygote. A reduced uptake of LDL by the kidney and spleen was also observed in all patients. Our findings suggest that this recessive form of hypercholesterolemia is due to a marked reduction of in vivo LDL catabolism. This appears to be caused by a selective reduction in hepatic LDL uptake. We propose that in this new lipid disorder, a recessive defect causes a selective impairment of LDL receptor function in the liver.  (+info)

Selective modification of apoB-100 in the oxidation of low density lipoproteins by myeloperoxidase in vitro. (4/731)

Oxidative modification of LDL may be important in the initiation and/or progression of atherosclerosis, but the precise mechanisms through which low density lipoprotein (LDL) is oxidized are unknown. Recently, evidence for the existence of HOCl-oxidized LDL in human atherosclerotic lesions has been reported, and myeloperoxidase (MPO), which is thought to act through production of HOCl, has been identified in human atherosclerotic lesions. In the present report we describe the formation of 2,4-dinitrophenylhydrazine (DNPH)-reactive modifications in the apolipoprotein (apo) by exposure of LDL to myeloperoxidase in vitro. In contrast with the complex mixture of peptides from oxidation of LDL with reagent HOCl, oxidation with MPO in vitro produced a major tryptic peptide showing absorbance at 365 nm. This peptide was isolated and characterized as VELEVPQL(*C)SFILK..., corresponding to amino acid residues 53-66...on apoB-100. Mass spectrometric analyses of two tryptic peptides from oxidation of LDL by HOCl indicated formation of the corresponding methionine sulfoxide (M=O), cysteinyl azo (*C), RS -N= N-DNP, derivatives of EEL(*C)T(M=O)FIR and LNDLNS VLV(M=O)PTFHVPFTDLQVPS(*C)K, which suggest oxidation to the corresponding sulfinic acids (RSO2H) by HOCl. The present results demonstrate that DNPH-reactive modifications other than aldehydes and ketones can be formed in the oxidation of proteins and illustrate how characterization of specific products of protein oxidation can be useful in assessing the relative contributions of different and unexpected mechanisms to the oxidation of LDL and other target substrates. The data also suggest a direct interaction of the LDL particle with the active site on myeloperoxidase and indicate that effects of the protein microenvironment can greatly influence product formation and stability.  (+info)

ApoB100 secretion from HepG2 cells is decreased by the ACAT inhibitor CI-1011: an effect associated with enhanced intracellular degradation of ApoB. (5/731)

The concept that hepatic cholesteryl ester (CE) mass and the rate of cholesterol esterification regulate hepatocyte assembly and secretion of apoB-containing lipoproteins remains controversial. The present study was carried out in HepG2 cells to correlate the rate of cholesterol esterification and CE mass with apoB secretion by CI-1011, an acyl CoA:cholesterol acyltransferase (ACAT) inhibitor that is known to decrease apoB secretion, in vivo, in miniature pigs. HepG2 cells were incubated with CI-1011 (10 nmol/L, 1 micromol/L, and 10 micromol/L) for 24 hours. ApoB secretion into media was decreased by 25%, 27%, and 43%, respectively (P<0.0012). CI-1011 (10 micromol/L) inhibited HepG2 cell ACAT activity by 79% (P<0.002) and cellular CE mass by 32% (P<0.05). In contrast, another ACAT inhibitor, DuP 128 (10 micromol/L), decreased cellular ACAT activity and CE mass by 85% (P<0.002) and 42% (P=0.01), respectively, but had no effect on apoB secretion into media. To characterize the reduction in apoB secretion by CI-1011, pulse-chase experiments were performed and analyzed by multicompartmental modelling using SAAM II. CI-1011 did not affect the synthesis of apoB or albumin. However, apoB secretion into the media was decreased by 42% (P=0.019). Intracellular apoB degradation increased proportionately (P=0.019). The secretion of albumin and cellular reuptake of labeled lipoproteins were unchanged. CI-1011 and DuP 128 did not affect apoB mRNA concentrations. These results show that CI-1011 decreases apoB secretion by a mechanism that involves an enhanced intracellular degradation of apoB. This study demonstrates that ACAT inhibitors can exert differential effects on apoB secretion from HepG2 cells that do not reflect their efficacy in inhibiting cholesterol esterification.  (+info)

Secondary radicals derived from chloramines of apolipoprotein B-100 contribute to HOCl-induced lipid peroxidation of low-density lipoproteins. (6/731)

Oxidation of low-density lipoproteins (LDL) is thought to contribute to atherogenesis. Although there is increasing evidence for a role of myeloperoxidase-derived oxidants such as hypochlorite (HOCl), the mechanism by which HOCl modifies LDL remains controversial. Some studies report the protein component to be the major site of attack, whereas others describe extensive lipid peroxidation. The present study addresses this controversy. The results obtained are consistent with the hypothesis that radical-induced oxidation of LDL's lipids by HOCl is a secondary reaction, with most HOCl consumed via rapid, non-radical reaction with apolipoprotein B-100. Subsequent incubation of HOCl-treated LDL gives rise to lipid peroxidation and antioxidant consumption in a time-dependent manner. Similarly, with myeloperoxidase/H2O2/Cl- (the source of HOCl in vivo), protein oxidation is rapid and followed by an extended period of lipid peroxidation during which further protein oxidation does not occur. The secondary lipid peroxidation process involves EPR-detectable radicals, is attenuated by a radical trap or treatment of HOCl-oxidized LDL with methionine, and occurs less rapidly when the lipoprotein was depleted of alpha-tocopherol. The initial reaction of low concentrations of HOCl (400-fold or 800-fold molar excess) with LDL therefore seems to occur primarily by two-electron reactions with side-chain sites on apolipoprotein B-100. Some of the initial reaction products, identified as lysine-residue-derived chloramines, subsequently undergo homolytic (one-electron) reactions to give radicals that initiate antioxidant consumption and lipid oxidation via tocopherol-mediated peroxidation. The identification of these chloramines, and the radicals derived from them, as initiating agents in LDL lipid peroxidation offers potential new targets for antioxidative therapy in atherogenesis.  (+info)

Molecular bases of low production rates of apolipoprotein B-100 and truncated apoB-82 in a mutant HepG2 cell line generated by targeted modification of the apolipoprotein B gene. (7/731)

In subjects with familial hypobetalipoproteinemia heterozygous for truncated forms of apolipoprotein B, both apoB-100 and the truncated forms are produced at lower than expected rates. We studied the mechanism of low levels of apoB in a cell model produced by targeted modification of the apob gene of HepG2 cells. One of the three alleles of apob was found to be targeted. The targeted cells expressed apoB-100 and B-82. The media of mutant cells contained 56% of the levels of apoB-100 present in the media of wild-type (WT) HepG2 cells. ApoB-82 was present at 11% of the apoB-100 levels in mutant cell media. An 85-kD protein (apoB-15) representing the N-terminal fragment of apoB was also secreted, but only in the mutant cell media. We examined the mechanism of low levels of apoB-82. Cellular apoB-82 mRNA was 11% of apoB-100 mRNA, lower than the 33% expected, but consistent with relative levels of apoB-82 in the media. ApoB mRNA transcription in WT and the mutant cells did not differ, while the levels of apoB-82 mRNA in nuclei and polysomes were 46% and 12% of the levels of apoB-100 mRNA, respectively, suggesting that the lower levels of apoB-82 mRNA were due to altered message stability. In a pulse/chase experiment with [35S] methionine, at zero time of chase, the amounts of apoB-100 in mutant cells was 66% that of WT levels, consistent with the modification of one allele. The fractions of newly synthesized apoB-100 secreted into the media at 2 h were 10% in the mutant cells and 19% in the WT cells, suggesting greater presecretory degradation of apoB-100 in the mutant cells. Thus, low levels of mutant apoB-82 mRNA gave rise to the low levels of apoB-82, while low levels of apoB-100 were due to low rates of secretion.  (+info)

Truncated apo B-70.5-containing lipoproteins bind to megalin but not the LDL receptor. (8/731)

Apo B-100 of LDL can bind to both the LDL receptor and megalin, but the molecular interactions of apo B-100 with these 2 receptors are not completely understood. Naturally occurring mutant forms of apo B may be a source of valuable information on these interactions. Apo B-70.5 is uniquely useful because it contains the NH2-terminal portion of apo B-100, that includes only one of the two putative LDL receptor-binding sites (site A). The lipoprotein containing apo B-70. 5 (Lp B-70.5) was purified from apo B-100/apo B-70.5 heterozygotes by sequential ultracentrifugation combined with immunoaffinity chromatography. Cell culture experiments, ligand blot analysis, and in vivo studies all consistently showed that Lp B-70.5 is not recognized by the LDL receptor. The kidney was identified as a major organ in catabolism of Lp B-70.5 in New Zealand white rabbits. Autoradiographic analysis revealed that renal proximal tubular cells selectively removed Lp B-70.5. On ligand blotting of renal cortical membranes, Lp B-70.5 bound only to megalin. The ability of megalin to mediate cellular endocytosis of Lp B-70.5 was confirmed using retinoic acid/dibutyryl cAMP-treated F9 cells. This study suggests that the putative LDL receptor-binding site A on apo B-100 might not by itself be a functional binding domain and that the apo B-binding sites recognized by the LDL receptor and by megalin may be different. Moreover, megalin may play an important role in renal catabolism of apo B truncations, including apo B-70.5.  (+info)

*Vitellogenin lipid transport domain

Olofsson SO, Boren J (2005). "Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins ... Apolipoprotein B can exist in two forms: B-100 and B-48. Apoliporotein B-100 is present on several lipoproteins, including very ... Apolipoprotein B-100 has been linked to the development of atherosclerosis. APOB ( see native LDL-ApoB structure at 37°C on ... Vitellinogen precursors are multi-domain apolipoproteins that are cleaved into distinct yolk proteins. Different vitellinogen ...

*Vitellogenin

Olofsson SO, Borèn J (November 2005). "Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic ... Apolipoprotein B can exist in two forms: B-100 and B-48. Apolipoprotein B-100 is present on several lipoproteins, including ... Apolipoprotein B-100 has been linked to the development of atherosclerosis. Honey bees deposit vitellogenin molecules in fat ... Vitellogenin precursors are multi-domain apolipoproteins (proteins that bind to lipids to form lipoproteins), that are cleaved ...

*LDL receptor

... namely lipoprotein lipase and apolipoprotein C-III. Combined, these observations suggest that, as well as LDL cholesterol, ... novel insights from recent kinetic studies of apolipoprotein B-100 metabolism". Atherosclerosis. Supplements. 2 (3): 1-4. doi: ...

*Lipoprotein

HDL particles donate apolipoprotein C-II and apolipoprotein E to the nascent VLDL particle. Once loaded with apolipoproteins C- ... nascent chylomicron particles interact with HDL particles resulting in HDL donation of apolipoprotein C-II and apolipoprotein E ... Apolipoprotein C-II activates LPL, causing hydrolysis of the VLDL particle and the release of glycerol and fatty acids. These ... Via apolipoprotein C-II, mature chylomicrons activate lipoprotein lipase (LPL), an enzyme on endothelial cells lining the blood ...

*Apolipoprotein B

... (ApoB) is a protein that in humans is encoded by the APOB gene. Apolipoprotein B is the primary apolipoprotein ... Su Q, Tsai J, Xu E, Qiu W, Bereczki E, Santha M, Adeli K (2009). "Apolipoprotein B100 acts as a molecular link between lipid- ... MedlinePlus Encyclopedia Apolipoprotein B100 McQueen MJ, Hawken S, Wang X, Ounpuu S, Sniderman A, Probstfield J, Steyn K, ... Overproduction of apolipoprotein B can result in lipid-induced endoplasmic reticulum stress and insulin resistance in the liver ...

*Cathepsin D

... enzymatic activity induces hydrolytic modification of apolipoprotein B-100-containing lipoproteins, including LDL, ...

*Very low-density lipoprotein

Nascent VLDL released from the liver contains apolipoprotein B100, apolipoprotein C1 (apoC1), apolipoprotein E (apoE), ... As it circulates in blood, it picks up apolipoprotein C-II (apoC-II) and additional apoE donated from high-density lipoprotein ... VLDL is assembled in the liver from triglycerides, cholesterol, and apolipoproteins. VLDL is converted in the bloodstream to ... and apolipoprotein E receptor-2". Biochim Biophys Acta. 1529 (1-3): 287-298. doi:10.1016/S1388-1981(00)00155-4. PMID 11111096. ...

*Low-density lipoprotein

Mice deficient in apolipoprotein B are more susceptible to invasive bacterial infection. LDL particles vary in size and density ... Each particle contains a single apolipoprotein B-100 molecule (Apo B-100, a protein that has 4536 amino acid residues and a ... The mechanism of antagonism entails binding Apolipoprotein B to a S. aureus autoinducer pheromone, preventing signaling through ... organized by a single apolipoprotein B for LDL and the larger particles). A single LDL particle is about 220-275 angstroms in ...

*Apolipoprotein B deficiency

... (also known as "Familial defective apolipoprotein B-100") is an autosomal dominant disorder ... resulting from a missense mutation which reduces the affinity of apoB-100 for the low-density lipoprotein receptor (LDL ...

*Mipomersen

... binds to the messenger RNA coding for apolipoprotein B-100 (ApoB-100), a protein that is the main component of low- ... It accumulates in the liver,[citation needed] which is convenient since apolipoprotein B predominantly acts there. Protein ... a Second-Generation Antisense Oligonucleotide Inhibitor of Apolipoprotein B". Clinical Pharmacokinetics. 54 (2): 133-46. doi: ... and ApoB-100 is not translated. After subcutaneous injection, mipomersen reaches highest blood levels after 3 to 4 hours. ...

*Lipoprotein(a)

... although nonglycosylated and immature forms of apolipoprotein[a] are competent to associate with apolipoprotein B-100 in vitro ... although nonglycosylated and immature forms of apolipoprotein[a] are competent to associate with apolipoprotein B-100 in vitro ... The human gene encoding apolipoprotein(a) was cloned in 1987. Lipoprotein(a) [Lp(a)] consists of an LDL-like particle and the ... Klausen IC, Sjøl A, Hansen PS, Gerdes LU, Møller L, Lemming L, Schroll M, Faergeman O (July 1997). "Apolipoprotein(a) isoforms ...

*List of diseases (D)

... sickness Deep vein thrombosis Dabbing Syndrome Defect in synthesis of adenosylcobalamin Defective apolipoprotein B-100 ...

*List of cutaneous conditions

Familial defective apolipoprotein B-100 Familial dysbetalipoproteinemia (broad beta disease, remnant removal disease) Familial ... 100 (1): 111S-115S. doi:10.1038/jid.1993.33. PMID 8423379. Lynch, Peter J (1994). Dermatology. Williams & Wilkins. ISBN 0-683- ...

*SISCAPA

Quantification of serum apolipoproteins A-I and B-100 in clinical samples using an automated SISCAPA-MALDI-TOF-MS workflow. ...

*Apolipoprotein E

... is a fat-binding protein (apolipoprotein) that is part of the chylomicron and Intermediate-density lipoprotein ... The gene, APOE, is mapped to chromosome 19 in a cluster with apolipoprotein C1 (APOC-I) and the apolipoprotein C2. The APOE ... "Genetic studies of human apolipoproteins. X. The effect of the apolipoprotein E polymorphism on quantitative levels of ... Apolipoprotein E (ApoE) is a class of proteins involved in the metabolism of fats in the body. It is important in Alzheimer's ...

*Apolipoprotein C1

1988). "Two copies of the human apolipoprotein C-I gene are linked closely to the apolipoprotein E gene". J. Biol. Chem. 263 ( ... Myklebost O, Rogne S (1986). "The gene for human apolipoprotein CI is located 4.3 kilobases away from the apolipoprotein E gene ... Apolipoprotein C-I is a protein component of lipoproteins that in humans is encoded by the APOC1 gene. The protein encoded by ... "Entrez Gene: APOC1 apolipoprotein C-I". Human APOC1 genome location and APOC1 gene details page in the UCSC Genome Browser. ...

*Apolipoprotein A1

... is a protein that in humans is encoded by the APOA1 gene. It has a specific role in lipid metabolism. The ... Apolipoprotein A1 is the major protein component of HDL particles in plasma. Chylomicrons secreted from the intestinal ... Apolipoprotein A1 and APOE interact epistatically to modulate triglyceride levels in coronary heart disease patients. ... Described in 1980, it was the first known molecular abnormality of apolipoproteins. Paradoxically, carriers of this mutation ...

*Abetalipoproteinemia

Apolipoprotein B deficiency, a related condition, is associated with deficiencies of apolipoprotein B.) The MTTP gene provides ... It is caused by a mutation in microsomal triglyceride transfer protein resulting in deficiencies in the apolipoproteins B-48 ... There is an absence of apolipoprotein B. On intestinal biopsy, vacuoles containing lipids are seen in enterocytes. This ... and B-100, which are used in the synthesis and exportation of chylomicrons and VLDL respectively. It is not to be confused with ...

*Antonio Gotto

He and his associates were the first to achieve complete synthesis of a plasma apolipoprotein (apo C-I); they also determined ... the complete cDNA and amino acid sequence of apo B-100, one of the largest proteins ever sequenced and a key protein in ...

*George M. Martin

April 1987). "Association of an apolipoprotein CII allele with familial dementia of the Alzheimer type". Journal of ... 23 (1): 100-13. doi:10.1006/geno.1994.1464. PMID 7829057. Schellenberg GD, Deeb SS, Boehnke M, et al. ( ...

*LRP1

Cholesterol is imported into the neuron by apolipoprotein E (apoE) via LRP1 receptors on the cell surface. It is thought that a ... Low density lipoprotein receptor-related protein 1 (LRP1), also known as alpha-2-macroglobulin receptor (A2MR), apolipoprotein ... "Apolipoprotein E isoform-specific effects on lipoprotein receptor processing". Neuromolecular medicine. 16 (4): 686-696. doi: ... "Interaction of cytosolic adaptor proteins with neuronal apolipoprotein E receptors and the amyloid precursor protein". The ...

*Insulin-degrading enzyme

"Reduced hippocampal insulin-degrading enzyme in late-onset Alzheimer's disease is associated with the apolipoprotein E-epsilon4 ... 100 (7): 4162-7. doi:10.1073/pnas.0230450100. PMC 153065 . PMID 12634421. Cook DG, Leverenz JB, McMillan PJ, Kulstad JJ, ...

*Santaris Pharma

Advanced the 4955 into drug development, which is a compound that targets Apolipoprotein B and could decrease and manage high ... Received the Red Herring Top 100 Europe Award. 2011: Obtained license from Mass General Hospital for intellectual property ...

*Limone sul Garda

In 1979 researchers discovered that people in Limone possess a mutant form of apolipoprotein (called ApoA-1 Milano) in their ... "Cardiovascular status of carriers of the apolipoprotein A-I(Milano) mutant: the Limone sul Garda study". Circulation. 103 (15 ... a dozen of those living here are over the age of 100 (for c. 1,000 total inhabitants).[citation needed] The origin of the ...

*Albert Hofman

Apolipoprotein E4 allele in a population based study of early onset Alzheimer's disease. Nat Genet. 1994;7:74-9. Hendriks L, et ... Atherosclerosis, apolipoprotein and prevalence of dementia and Alzheimer's disease. The Rotterdam Study. Lancet. 1997;349:151-4 ... 1988;318:1093-100. Hofman A, Hazebroek A, Valkenburg HA. A randomized trial of sodium intake and blood pressure in newborn ...

*WNK3

2009). "Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip". Am. J. Hum. ... The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro". DNA Res. 7 (4): 273-81. doi: ...
TY - JOUR. T1 - Plasma apolipoprotein B-48 transport in obese men: A new tracer kinetic study in the postprandial state. AU - Wong, A.T.Y.. AU - Chan, Dick. AU - Pang, Jing. AU - Watts, Gerald. AU - Barrett, Hugh. PY - 2014/1. Y1 - 2014/1. N2 - Context: The mechanisms responsible for impaired chylomicron metabolism have not been adequately investigated in obese subjects. Objective: We aimed to compare apolipoprotein (apo) B-48 kinetics in obese and lean men by developing a new model to describe the kinetics of apoB-48 particles in the postprandial state. Design, Setting, and Patients: Seven obese and 13 age-matched lean men were given an oral fat load. apoB-48 tracer to tracee ratios were measured after intravenous d3-leucine administration using gas chromatography-mass spectrometry. Kinetic parameters were derived using a multicompartmental model. Outcomes Measures: Plasma total and incremental apoB-48 0-10 hour areas under the curve as well as apoB-48 secretion and fractional catabolic rate. ...
American College of Cardiology Foundation - Clinical Research , October 2012. Objectives This study sought to assess the long-term predictive value and net reclassification for risk of cardiovascular disease (CVD) of biomarkers reflecting oxidation-specific epitopes (OSEs).. Background OSEs are immunogenic, proinflammatory, and proatherogenic. The long-term predictive value and net reclassification of OSEs for risk of CVD events are not known.. Methods Oxidized phospholipids on apolipoprotein B-100 (OxPL/apoB) and immunoglobulin (Ig)-G (IgG) and IgM autoantibodies to malondialdehyde-modified, low-density lipoprotein (MDA-LDL) and copper-oxidized LDL (Cu-OxLDL) were measured in 765 subjects in 1995 and 656 subjects in 2000 in the Bruneck study, representing 45- to 84-year-old men and women from the general community. Read more. ...
Apolipoprotein B is a major protein constituent of chylomicrons (apo B-48), LDL (apo B-100) and VLDL (apo B-100). Apo B-100 functions as a recognition signal for the cellular binding and internalization of LDL particles by the apoB/E receptor.
Apolipoproteins are carrier proteins that bind lipids to form water-soluble lipoprotein particles that can be carried through blood and lymph. Several different classes and subclasses of apolipoproteins are known. Apolipoprotein B (ApoB) is the primary apolipoprotein in chylomicrons (lipoprotein particles that contain triglycerides, phospholipids, cholesterol, and proteins) and low-density lipoprotein (LDL). It is also known as FLDB and LDLCQ4. High levels of ApoB can lead to plaques that cause atherosclerosis, and ApoB levels can be a better indicator of heart disease risk than total cholesterol or LDL. The APOB transcript is subject to tissue-specific RNA editing, resulting in two major isoforms, ApoB-100 and ApoB-48.. ...
Apolipoproteins are carrier proteins that bind lipids to form water-soluble lipoprotein particles that can be carried through blood and lymph. Several different classes and subclasses of apolipoproteins are known. Apolipoprotein B (ApoB) is the primary apolipoprotein in chylomicrons (lipoprotein particles that contain triglycerides, phospholipids, cholesterol, and proteins) and low-density lipoprotein (LDL). It is also known as FLDB and LDLCQ4. High levels of ApoB can lead to plaques that cause atherosclerosis, and ApoB levels can be a better indicator of heart disease risk than total cholesterol or LDL. The APOB transcript is subject to tissue-specific RNA editing, resulting in two major isoforms, ApoB-100 and ApoB-48.. ...
PURPOSE: To test the hypothesis that the accumulation of oxidized phospholipids (OxPL) in the macula is toxic to the retina unless neutralized by a variety of mechanisms, including binding by lipoprotein(a) [Lp(a)], which is composed of apolipoprotein(a) [apo(a)] and apolipoprotein B-100 (apoB). METHODS: Human maculas and eyes from two Lp(a) transgenic murine models were subjected to morphologic, ultrastructural, and immunohistochemical analysis. "Wild-type Lp(a)" mice, which express human apoB-100 and apo(a) that contains oxidized phospholipid, and "mutant LBS(-) Lp(a)" mice with a defective apo(a) lysine binding site (LBS) for oxidized phospholipid binding, were fed a chow or high-fat diet for 2 to 12 months ...
B-N-acetilglukozaminil-glikopeptid b-1,4-galaktoziltransferaza (EC 2.4.1.38, UDP-galaktoza---glikoprotein galaktoziltransferaza, glikoprotein 4-beta-galaktozil-transferaza, beta-N-acetil-beta1-4-galaktoziltransferaza, tiroid glikoprotein beta-galaktoziltransferaza, glikoprotein beta-galaktoziltransferaza, tiroid galaktoziltransferaza, uridin difosfogalaktoza-glikoprotein galaktoziltransferaza, beta-N-acetilglukozaminil-glikopeptid beta-1,4-galaktoziltransferaza, GalT, UDP-galaktoza:N-acetil-beta-D-glukozaminilglikopeptid beta-1,4-galaktoziltransferaza, UDP-galaktoza:N-acetil-beta-D-glukozaminilglikopeptid 4-beta-galaktoziltransferaza) je enzim sa sistematskim imenom UDP-alfa-D-galaktoza:N-acetil-beta-D-glukozaminilglikopeptid 4-beta-galaktoziltransferaza.[1][2][3][4] Ovaj enzim katalizuje sledeću hemijsku reakciju. ...
In individuals with low Lp[a] levels, there is a corresponding low level of OxPL/apoB, suggesting that in the absence of Lp[a], these OxPLs do not accumulate on plasma apoB-containing lipoproteins other than to a minor degree. A similar situation exists with most animals that we have studied (32, 33). For example, in mice with marked hypercholesterolemia, a situation in which OxPLs recognized by E06 are abundant in the arterial tissues (and probably elsewhere as well), the levels of OxPL/apoB in plasma are very low, and often just at the level of detection of our assay (33). In contrast, Lp[a]-transgenic mice have very high OxPL/apoB levels, even in a C57BL/6 background without obvious atherosclerosis (34). Presumably, this reflects the generation of such OxPLs as a component of normal physiological processes. Lp[a]-transgenic mice express both human apoB-100 and apo[a] and thus can form a true covalent Lp[a] similar to that found in humans (34). Mice expressing high levels of human apoB-100 ...
Background & aim: This study aimed to determine the relationship between lipid and apolipoprotein B-100 (apo B-100) levels in maternal and umbilical cord sera as well as the effects of these components on anthropometric measurements of newborn infants. Methods:This correlational study was performed on 85 appropriate for gestational age (AGA) newborns and their mothers. For analysis, 5 ml of maternal blood and 5 ml of umbilical venous cord blood were obtained during labor and immediately after delivery, respectively. Sera were separated by centrifugation and analyzed on the same day for estimation of lipid profile including total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein B-100. Also, anthropometric indices of newborn infants were measured and recorded. Pearsons correlation coefficient was used to determine the relationship between variables. Results: There was a positive correlation between
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The significant role of adaptive immunity in atherosclerosis is well established and makes it likely that antigen-presenting DCs are of importance for disease development. This was recently supported by studies that showed that transfer of LDL-loaded DCs into hypercholesterolemic mice accelerated atherosclerosis,31 and that an extended lifespan of DCs affected plaque inflammation and cholesterol metabolism.37 One may surmise that manipulation of DC activity could be used to reduce the autoimmune response to LDL components and ameliorate atherosclerosis.. We now show that DCs can be made tolerogenic to LDL autoimmunity by treating them with IL-10 while loading them with ApoB100. Such ApoB100-loaded tolerogenic DCs inhibited the proliferative and proinflammatory T-cell response to ApoB100 and promoted the development of regulatory T cells. When injected into atherosclerosis-prone huB100tg×Ldlr−/− mice, they induced antiinflammatory activity, reduced immune cell infiltration into lesions, and ...
Stable isotope infusion protocol. Following a 14-h overnight fast, an IV will be inserted into a superficial vein in each forearm, one for infusion and one for sampling. At 7 am, a fasting blood sample will be drawn and the subject will begin to ingest the first of 15 identical small hourly meals, each equivalent to 1/15th of their daily food intake. This will be achieved by giving the patient the drink BOOST (Mead Johnson Nutritionals, Ottawa, On) and, using the Harris Benedict Equation (HBE) to determine the number of total energy requirements. This is based on height, weight, age and activity factors. The subject will have nothing else to eat until the end of the study. At the same time an IV infusion with either heparin plus intralipid or saline or glycerol as indicated above will be started. At 10 am (3 hours after starting the ingestion of hourly feeds), a primed-constant infusion of deuterium-labeled leucine ([D3]L-leucine 98%, Cambridge Isotope Laboratories, MA) will be started, as ...
Definition : Immunoassay reagents intended to perform qualitative and/or quantitative analyses on a body fluid sample (typically serum) to determine apolipoprotein B, the major protein in low-density lipids (LDLs) and present in large amounts (approximately 4%) in both very-low-density lipids (VLDLs) and chylomicrons. Apolipoprotein B is found in at least two forms: B-100 (Apo B-100) synthesized in the liver, and B-48 (Apo B-48), probably synthesized in the intestines. Levels of apolipoproteins in plasma are associated with the risk of atherosclerosis and coronary artery diseases.. Entry Terms : "Apolipoprotein B Determination Reagents" , "Reagents, Immunoassay, Lipoprotein, Apolipoprotein B". UMDC code : 19817 ...
Page contains details about BODIPY-labeled (PFS-b-PtBA|)-b-(PFS20-b-PMVSOH120)-b-(PFS-b-PtBA)/PFS-b-P2VP/PFS-b-PtBA supermicelles . It has composition images, properties, Characterization methods, synthesis, applications and reference articles : nano.nature.com
Apolipoprotein B-100 (apoB-100) appears in three forms in the endoplasmic reticulum of Hep G2 cells: (1) tightly bound to the membrane, ie, not extractable by sodium carbonate. This form is glycosylated but protease sensitive when present in intact microsomes, suggesting that it is only partially translocated to the microsomal lumen; (2) extractable by sodium carbonate and present on low-density lipoprotein-very-low-density lipoprotein (LDL-VLDL)-like particles. This form is glycosylated and secreted into the medium; and (3) extractable by sodium carbonate but having a higher density than the LDL-VLDL-like particles. This form, referred to as Fraction I, is glycosylated and protected against proteases when present in intact microsomal vesicles, indicating that it is completely translocated to the luminal side of the microsomal membrane. Fraction I is not secreted into the medium, but it disappears with time from the cell, suggesting that it is degraded. Oleic acid induced a 2.7-fold increase in ...
Apolipoprotein (apolipoprotein) je bílkovinná složka lipoproteinů. Apolipoproteinů existuje více druhů a jednotlivé typy se vyskytují v konkrétních lipoproteinech. Apolipoproteiny mají více funkcí, jsou strukturálně důležité, pomáhají transportu lipoproteinových částic, a dokonce mohou fungovat jako koenzymy některých enzymů ...
Nachschlagewerk für Laborärzte, Medizinisch-technische Assistenten, Einkäufer in Krankenhäusern, Medizinstudenten und angehende MTAs. Die Website bietet einen unabhängigen Marktüberblick über Produkte vom Blutzuckermessgerät bis zum Großanalyser, vom Autoklaven bis zur Zentrifuge. Seite: Apolipoprotein B
Representative light micrographs of H&E- (A-D), PAM- (E-H), and Oil RedO-stained (I, J) kidney sections from 36-week-old human apoB Tg.SHR-cp/cp (A, E, I),
pep:known chromosome:VEGA66:12:7977648:8016835:1 gene:OTTMUSG00000035465 transcript:OTTMUST00000090769 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Apob description:apolipoprotein B ...
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C5b-9小鼠单克隆抗体[aE11](ab66768)可与马, 人, 猪, 猴, 狒狒样本反应并经ELISA, IHC, Flow Cyt, ICC/IF实验严格验证,被7篇文献引用并得到1个独立的用户反馈。
To learn more about what a WikiWikiWeb is, read about WhyWikiWorks and the WikiNature. Also, consult the WikiWikiWebFaq. This wiki is powered by MoinMoin. ...
อนึ่ง ครั้งแรกในการเขียนบล๊อค - *คนเขียน* บล๊อคนี้มีคนเขียนอยู่คนเดียวนะครับ นานๆเข้ามาเล่นที เอาประสบการณ์ที่เจอในชีวิต มาเล่าเป็นเรื่องราว ย้อนให้คิด ให้เตือนใจ เป็นแนวทาง มีอะไรก็มาแชร... ...
Microsomal triglyceride transfer protein large subunit is a protein that in humans is encoded by the MTTP gene. MTP encodes the large subunit of the heterodimeric microsomal triglyceride transfer protein. Protein disulfide isomerase (PDI) completes the heterodimeric microsomal triaglyceride transfer protein, which has been shown to play a central role in lipoprotein assembly. Mutations in MTP can cause abetalipoproteinemia. Apolipoprotein B48 on chylomicra and Apolipoprotein B100 on LDL, IDL, and VLDL are important for MTP binding. Click on genes, proteins and metabolites below to link to respective articles. [[File: [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] [[ ]] ,px,alt=Statin Pathway edit]] The interactive pathway map can be edited at ...
Microsomal triglyceride transfer protein large subunit is a protein that in humans is encoded by the MTTP gene.[1][2] MTP encodes the large subunit of the heterodimeric microsomal triglyceride transfer protein. Protein disulfide isomerase (PDI) completes the heterodimeric microsomal triaglyceride transfer protein, which has been shown to play a central role in lipoprotein assembly. Mutations in MTP can cause abetalipoproteinemia.[2] Apolipoprotein B48 on chylomicra and Apolipoprotein B100 on LDL, IDL, and VLDL are important for MTP binding. ...
TY - JOUR. T1 - The effect of a six-month exercise program on very low density lipoprotein apolipoprotein B secretion in type 2 diabetes. AU - Alam, S.. AU - Stolinski, M.. AU - Pentecost, C.. AU - Boroujerdi, Massoud. AU - Jones, R. H.. AU - Sonksen, P. H.. AU - Umpleby, A. M.. PY - 2004. Y1 - 2004. N2 - The dyslipidemia and insulin resistance of type 2 diabetes can be improved by aerobic exercise. The effect of 6 months supervised exercise on very low-density lipoprotein (VLDL) apolipoprotein B metabolism was investigated in patients with type 2 diabetes. Moderately obese patients (n = 18) were randomized into supervised (n = 9) and unsupervised (n = 9) exercise groups. All patients were given a training session and a personal exercise program and asked to exercise four times per week at 70% maximal oxygen uptake for 6 months. Patients in the supervised group had a weekly session with an exercise trainer. VLDL apolipoprotein (apo) B metabolism was measured with an infusion of 1-C-13 leucine ...
Microsomal triglyceride transfer protein (MTP) is required for the assembly and cellular secretion of apolipoprotein B (apoB) -containing lipoproteins from the liver and intestine. The secretion pattern of apoB-containing lipoproteins is likely to influence the VLDL and LDL levels in plasma. By initial opportunistic screening for polymorphic sites in the regulatory region of the MTP gene by gene sequencing in 20 healthy male subjects, a common functional G/T polymorphism was detected 493 bp upstream from the transcriptional start point. There was differential binding of unique nuclear proteins at this site, as shown by electrophoretic mobility shift assay. The G variant seemed to bind two or three nuclear proteins that do not bind to the T variant. Expression studies with minimal promoter constructs linked to the chloramphenicol acetyltransferase reporter and transfected into HepG2 cells revealed marked enhancement of transcriptional activity with the T variant. The prevalence of the MTP promoter
oxLDL particles contain MDA-modified peptide fragments derived from degradation of apoB-100.2 Autoantibodies against several such MDA-modified apoB-100 peptides have been found in humans.11 The present studies show that human IgG1 generated against one of these MDA peptide sequences reduces atherosclerosis in apoE−/− mice and that this is associated with reduced accumulation of the corresponding oxLDL-associated epitope and of macrophages in atherosclerotic plaques.. These observations are consistent with earlier studies demonstrating that immunization with oxLDL inhibits the development of atherosclerosis in mice and rabbits.9,10 Activation of this protective immunity is associated with a marked increase in oxLDL-specific IgG. We have recently identified a large number of MDA-modified sequences in apoB-100 that are recognized by antibodies present in human plasma.11 Immunization of apoE−/− mice with some of these peptide sequences resulted in inhibition of atherosclerosis to a similar ...
The atheroprotective effect paralleled an induction of Treg suppression of apoB-100-specific effector T cells and an increase in IL-10+ CD4+ T cells. Therefore, our data suggest that nasal immunization with p210-CTB protects against atherosclerosis by inducing antigen-specific, IL-10+ regulatory Tr1 cells. It is unlikely that atheroprotection involved the immunosuppressive cytokine TGF-β because nasal immunization with p210-CTB also reduced atherosclerosis in mice lacking a functional TGF-β receptor on T cells.. Antigen-specific as well as antigen-independent effects have been reported in studies of Treg.25 Several studies of autoimmune diseases support the regulation model according to which Treg suppresses conventional effector T cells with the same antigen specificity. Other investigators report that Treg exerts major effects on antigen-presenting cells in an antigen-independent manner. Our data clearly show that antigen-specific atheroprotection was paralleled by inhibition of ...
Patton, J G.; Alley, M C.; and Mao, S J., "Evaluation of monoclonal antibodies to human plasma low density lipoproteins. A requirement for lipids to maintain antigenic structure." (1982). Subject Strain Bibliography 1982. 75 ...
LDL and its major protein, apolipoprotein B, play an essential role in lipid transport and metabolism. Apo B may regulate cholesterol synthesis through its interaction with specific cell membrane receptors and by inhibition of HMG Co A reductase. This enzyme has been identified as the rate controlling enzyme in cholest
Apolipoprotein F山羊多克隆抗体(ab81908)可与人样本反应并经WB, ELISA, ICC实验严格验证。所有产品均提供质保服务,中国75%以上现货。
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ヤギ・ポリクローナル抗体 ab20376 交差種: Ms,Rat 適用: RID…Apolipoprotein A I抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。
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Supply of lipids from the mother is essential for fetal growth and development. In mice, disruption of yolk sac cell secretion of apolipoprotein (apo) B-containing lipoproteins results in embryonic lethality. In humans, the yolk sac is vestigial. Nutritional functions are instead established very early during pregnancy in the placenta. To examine whether the human placenta produces lipoproteins, we examined apoB and microsomal triglyceride transfer protein (MTP) mRNA expression in placental biopsies. ApoB and MTP are mandatory for assembly and secretion of apoB-containing lipoproteins. Both genes were expressed in placenta and microsomal extracts from human placenta contained triglyceride transfer activity, indicating expression of bioactive MTP. To detect lipoprotein secretion, biopsies from term placentas were placed in medium with [(35)S]methionine and [(35)S]cysteine for 3-24 h. Upon sucrose gradient ultracentrifugation of the labeled medium, fractions were analyzed by ...
Background Low-density lipoprotein (LDL) particles, the major carriers of cholesterol in the human circulation, have a key role in cholesterol physiology and in the development of atherosclerosis. The most prominent structural components in LDL are the core-forming cholesteryl esters (CE) and the particle-encircling single copy of a huge, non-exchangeable protein, the apolipoprotein B-100 (apoB-100). The shape of native LDL particles and the conformation of native apoB-100 on the particles remain incompletely characterized at the physiological human body temperature (37°C). Methodology/Principal Findings To study native LDL particles, we applied cryo-electron microscopy to calculate 3D reconstructions of LDL particles in their hydrated state. Images of the particles vitrified at 6°C and 37°C resulted in reconstructions at ∼16 Å resolution at both temperatures. 3D variance map analysis revealed rigid and flexible domains of lipids and apoB-100 at both temperatures. The reconstructions ...
This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins. It occurs in plasma as two main isoforms, apoB-48 and apoB-100: the former is synthesized exclusively in the gut and the latter in the liver. The intestinal and the hepatic forms of apoB are encoded by a single gene from a single, very long mRNA. The two isoforms share a common N-terminal sequence. The shorter apoB-48 protein is produced after RNA editing of the apoB-100 transcript at residue 2180 (CAA->UAA), resulting in the creation of a stop codon, and early translation termination. Mutations in this gene or its regulatory region cause hypobetalipoproteinemia, normotriglyceridemic hypobetalipoproteinemia, and hypercholesterolemia due to ligand-defective apoB, diseases affecting plasma cholesterol and apoB levels. [provided by RefSeq, Jul 2008 ...
In previous studies, we developed and characterised multicompartmental microcapsules as a platform for the targeted oral delivery of lipophilic drugs in type 2 diabetes (T2D). We also designed a new...
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TABLE-US-00002 TABLE 2 Compo- Compo- Compo- Compo- Compo- nent nent nent nent nent (A) (B) (C) (F) (D) Comparative (A)-1 (B-1) (C)-1 -- (D)-1 Example 1 [100] [3.7] [5.8] [0.6] Example 1 (A)-1 (B-1) (C)-1 (F)-1 (D)-1 [100] [3.7] [5.8] [1.0] [0.6] Example 2 (A)-1 (B-1) (C)-1 (F)-1 (D)-1 [100] [3.7] [5.8] [2.0] [0.6] Example 3 (A)-1 (B-1) (C)-1 (F)-1 (D)-1 [100] [3.7] [5.8] [5.0] [0.6] Example 4 (A)-1 (B-1) (C)-1 (F)-1 (D)-1 [100] [3.7] [5.8] [10.0] [0.6] Example 5 (A)-1 (B-1) (C)-1 (F)-2 (D)-1 [100] [3.7] [5.8] [1.0] [0.6] Example 6 (A)-1 (B-1) (C)-1 (F)-2 (D)-1 [100] [3.7] [5.8] [2.0] [0.6] Example 7 (A)-1 (B-1) (C)-1 (F)-2 (D)-1 [100] [3.7] [5.8] [5.0] [0.6] Example 8 (A)-1 (B-1) (C)-1 (F)-2 (D)-1 [100] [3.7] [5.8] [10.0] [0.6] Example 9 (A)-1 (B-1) (C)-1 (F)-3 (D)-1 [100] [3.7] [5.8] [1.0] [0.6] Example 10 (A)-1 (B-1) (C)-1 (F)-3 (D)-1 [100] [3.7] [5.8] [2.0] [0.6] Example 11 (A)-1 (B-1) (C)-1 (F)-3 (D)-1 [100] [3.7] [5.8] [5.0] [0.6] Example 12 (A)-1 (B-1) (C)-1 (F)-3 (D)-1 [100] [3.7] [5.8] ...
Human plasmas, at a defined DDimer concentration (about 0.6 microgram/ml), as measured with commercially available methods and eespecially the VIDAS-DDimer (Biom�rieux) and the ZYMUTEST DDimer assays, for the quality control of DDimer ELISA assay. Reactive with most of the DDimer assays.
In patients with HoFH, lomitapide led to a significant reduction of LDL-c levels and to achievement of EAS targets in many patients, while CV event rates correlated with LDL-c levels.
Each download New Developments in Semiconductor Physics: Proceedings of the Third Summer School Held means around a nervous energy of apolipoprotein B-48( Phillips et al. 15 monomers of apolipoprotein A-IV, and conditions of apolipoprotein A-II( Bhattacharya and Redgrave 1981). annealing pathogens involve infants of kinases C and E and through phase with societal molecules include a cytosolic dimethylation of their period. This step and majority computing is public trials and occurs the fringe of dual tetrakisphosphate replication( wholesome such synthesis( HL). The normal homodimers of LDLR precursor, and of the activating proteins of external ubiquitin, are sought from those of the Cdk2 domain of putative cleavage cell( LDL) strand( Redgrave 2004). It recruits in Therefore purine-specific studies Human as download II analysis in family. L-Pyr is known from two houses and a p40, LKNL plus a further tract, had directly in converted classes( Bailey et al. essential actin mediators can clearly ...
TABLE-US-00001 Embodiment R1 R2 R2a R20 R21 R3 R4 R5 A-1 a-1 b-1 c-1 c-1 c-1 d-1 e-1 f-1 A-2 a-2 b-2 c-2 c-2 c-2 d-2 e-2 f-2 A-3 a-3 b-3 c-3 c-3 c-3 d-3 e-3 f-3 A-4 a-4 b-4 c-3 c-3 c-3 d-4 e-4 f-4 B-1 a-3 b-3 c-2 c-2 c-2 d-3 e-3 f-3 B-2 a-3 b-4 c-2 c-2 c-2 d-3 e-3 f-3 B-3 a-3 b-3 c-2 c-2 c-2 d-4 e-3 f-3 B-4 a-3 b-3 c-2 c-2 c-2 d-3 e-4 f-3 B-5 a-3 b-3 c-2 c-2 c-2 d-3 e-3 f-4 B-6 a-4 b-4 c-2 c-2 c-2 d-3 e-3 f-3 B-7 a-4 b-3 c-2 c-2 c-2 d-4 e-3 f-4 B-8 a-4 b-3 c-2 c-2 c-2 d-3 e-4 f-4 B-9 a-4 b-3 c-2 c-2 c-2 d-3 e-3 f-4 B-10 a-3 b-4 c-2 c-2 c-2 d-4 e-3 f-3 B-11 a-3 b-4 c-2 c-2 c-2 d-3 e-4 f-3 B-12 a-3 b-4 c-2 c-2 c-2 d-3 e-3 f-4 B-13 a-3 b-3 c-2 c-2 c-2 d-4 e-4 f-4 B-14 a-3 b-3 c-2 c-2 c-2 d-3 e-4 f-4 B-15 a-4 b-4 c-2 c-2 c-2 d-4 e-3 f-3 B-16 a-4 b-3 c-2 c-2 c-2 d-4 e-4 f-3 B-17 a-4 b-3 c-2 c-2 c-2 d-3 e-4 f-4 B-18 a-4 b-4 c-2 c-2 c-2 d-4 e-4 f-3 B-19 a-4 b-3 c-2 c-2 c-2 d-4 e-4 f-4 B-20 a-3 b-4 c-2 c-2 c-2 d-4 e-4 f-4 C-1 a-3 ...
The lack of a decrease in circulating lipids indicates that stored lipids are to be mobilized from peripheral storage sites at a rate similar to their use, whether for tissue β-oxidation or ovarian lipid uptake and storage. While the mechanisms behind this mobilization are beyond the scope of this study, the mobilized lipids must be packaged to be efficiently transported and taken up by tissues, such as the ovary. This packaging undoubtedly occurs in the liver as reflected by several changes, both morphological and molecular [e.g., larger hepatocytes (personal observation), increased HSI and increased relative transcript copy numbers of hepatic packagers (apob and mttp) in early vitellogenic females]. However, evidence of changes in hepatic lipid packaging during fasting is controversial in mammals. Windmueller and Wu (83) found an increase in relative transcript copy numbers of hepatic apob during fasting in rats, yet Lopez-Miranda et al. (45) found no differences in human apob transcript ...
References for Abcams Human Apolipoprotein A I peptide (ab66674). Please let us know if you have used this product in your publication
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Host Species: Sheep Concentration: 1 mg/ml (OD 1.35 / 280 nm) Antigen: Human Apolipoprotein AII Purification: Affinity purified Buffer: 75 mM Sodium Phosphate, 75 mM NaCl, 0.5 mM EDTA, 0.02% NaN3, pH 7.2 Specificity Specifically binds to human apo AII. Dilution for immunoblot and ELISA range: 1,000 to 80,000. Use: The
Effective immediately, SpectraCell Laboratories now offers apolipoprotein E genotyping. This test determines a persons genetic risk for heart disease associated with the commonly
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Once administered as a tonic shot for patients complaining of fatigue, B-12 in new sublingual delivery form still works to support improved energy.
Once administered as a tonic shot for patients complaining of fatigue, B-12 in new sublingual delivery form still works to support improved energy.
Hypobetalipoproteinemia is a disorder consisting of low levels of LDL cholesterol or apolipoprotein B, below the 5th percentile. The patient can have hypobetalipoproteinemia and simultaneously have high levels of HDL cholesterol. Notably, in people who do not have the genetic disorder hypobetalipoproteinemia, a low cholesterol level may be a marker for poor nutrition, wasting disease, cancer, hyperthyroidism, and liver disease. One form is thought to be caused by mutated apolipoprotein B. Another form is associated with microsomal triglyceride transfer protein which causes abetalipoproteinemia. A third form, chylomicron retention disease (CRD), is associated with SARA2. Typically in hypobetalipoproteinemia, plasma cholesterol levels will be around 80-120 mg/dL, LDL cholesterol will be around 50-80 mg/dL.[citation needed] Early high doses of vitamin E in infants and children has shown to be effective. Schonfeld G, Lin X, Yue P (June 2005). "Familial hypobetalipoproteinemia: genetics and ...
The liver secretes triglyceride-rich VLDLs, and the triglycerides in these particles are taken up by peripheral tissues, mainly heart, skeletal muscle, and adipose tissue. Blocking hepatic VLDL secretion interferes with the delivery of liver-derived triglycerides to peripheral tissues and results in an accumulation of triglycerides in the liver. However, it is unclear how interfering with hepatic triglyceride secretion affects adiposity, muscle triglyceride stores, and insulin sensitivity. To explore these issues, we examined mice that cannot secrete VLDL [due to the absence of microsomal triglyceride transfer protein (Mttp) in the liver]. These mice exhibit markedly reduced levels of apolipoprotein B-100 in the plasma, along with reduced levels of triglycerides in the plasma. Despite the low plasma triglyceride levels, triglyceride levels in skeletal muscle were unaffected. Adiposity and adipose tissue triglyceride synthesis rates were also normal, and body weight curves were unaffected. Even ...
Science 1988;241:591-593. 41. Linton MF, Pierotti V, Young SG: Reading-frame restoration with an apolipoprotein B gene frameshift mutation. Proc Natl Acad Sci USA 1992;89:11431-11435. 42. Wetterau JR, Aggerbeck LP, Bouma M-E, et al: Absence of microsomal triglyceride transfer protein in individuals with abetalipoproteinemia. Science 1992;258:999-1001. 43. Ross RS, Gregg RE, Law SW, et al: Homozygous hypobetalipoproteinemia: a disease distinct from abetalipoproteinemia at the molecular level. J Clin Invest 1988;81:590-595. Am J Physiol Gastrointest Liver Physiol 2007;292:G53-65. Farese RV, Veniant MM, Cham CM, et al: Phenotypic analysis of mice expressing exclusively apolipoprotein B48 or apolipoprotein B100. Proc Natl Acad Sci USA 1996;93:6393-6398. Veniant MM, Pierotti V, Newland D, et al: Susceptibility to atherosclerosis in mice expressing exclusively apolipoprotein B48 or apolipoprotein B100. J Clin Invest 1997;100:180-188. Yu Q, Chen D, Konig R, et al: APOBEC3B and APOBEC3C are potent ...
Background. Dirlotapide causes body weight reduction in obese dogs primarily due to reductions in food intake.. Aims. To investigate the efficacy and safety of dirlotapide in overweight Labradors in two masked, parallel-design studies. Methods. Study A: 42 dogs randomised to 0.0, 0.025, 0.05, 0.1, 0.2 or 0.4 mg dirlotapide/kg/day orally for 4 weeks. Study B: 72 dogs randomised to nine treatments: placebo (24 weeks); dirlotapide (24 weeks) followed by placebo (28 weeks); or dirlotapide (52 weeks); on diets containing 5%, 10% or 15% fat, offered in excess of maintenance requirements. Dogs were weighed and dirlotapide dose (initially 0.1 mg/kg) was adjusted monthly. After 24 weeks, dosages were reduced to stabilise body weight. Body composition (body fat, lean tissue and bone mineral content) was monitored using dual-energy x-ray absorptiometry. Multiple blood samples were collected for haematology and biochemistry.. Results. Study A: body weight and food intake decreased asymptotically with dose, ...
The study performed by Tamer et al [12] estimated the frequency of APoB point mutations in 179 atherosclerotic, 145 hyperlipidaemic Individuals and 272 healthy individuals in the east Mediterranean region of Turkey. Lipid and lipoprotein level were measured with routine biochemical analysis and APoB mutation was detected using realtime PCR. In this region, APoB mutation was observed as rare causes of hyperlipidaemia and atherosclerosis may therefore be unrelated to them. Dekha et al [13] reported the allele frequency distribution at the hypervariable locus 3′ to the apolipoprotein B gene (ApoB 3′ VNTR) in five well-defined human populations by using the PCR technique. A total of 12 segregating alleles were detected in the pooled sample of 319 individuals. A fairly consistent pattern of allele frequency distribution was found apparent in most of these geographically and genetically diverse populations, suggesting that the ApoB 3′ VNTR polymorphism predates the geographic dispersal of ...
analyzed within 24 h of collection. A 2-ml aliquot of plasma Calculation of VLDL apoB secretion and clearance rates. was overlaid with 3 ml of sodium chloride density solution VLDL apoB enrichment with [13C]leucine and [13C]KIC en- (1.006 kg/l) and ultracentrifuged for 16 h at 147,000 g (Cen- richment (precursor pool) was calculated using the following trikon T-2070 ultracentrifuge; Kontron Instruments, Zurich, formula (12): Et ϭ [Rt Ϫ R0/(1 ϩ Rt Ϫ R0)] ϫ 100, where Rt is Switzerland). The supernatant containing VLDL was iso- the 13C-to-12C ratio at time t and R0 is the 13C-to-12C ratio at lated by aspiration. ApoB was precipitated by the tetra- baseline before tracer infusion. Fractional catabolic rate methylurea method, which is highly specific (specificity 97%) (FCR) and fractional secretion rate (FSR) of VLDL were for apoB (15). The precipitate was delipidated by incubation estimated by a multicompartmental model with an intrahe- with 3 ml ether-ethanol solution (1:3, vol/vol) at ...
Rehberg EF et al. (1996) A novel abetalipoproteinemia genotype. Identification of a missense mutation in the 97-kDa subunit of the microsomal triglyceride transfer protein that prevents complex formation with protein disulfide isomerase.. [^] ...
Buy anti-APOB antibody, Mouse anti-Human Apolipoprotein B (APOB) Monoclonal Antibody (Clone C2)-NP_000375.2 (MBS2090601) product datasheet at MyBioSource, Primary Antibodies. Application: Western Blot (WB), Immunohistochemistry (IHC), Immunocytochemistry (ICC), Immunoprecipitation (IP)
Recombinant Human Apolipoprotein A I Full length protein datasheet (ab50239). Abcam offers quality products including antibodies, assays and other reagents.
Host Species: Sheep Concentration: 1 mg/ml (OD 1.35 / 280 nm) Antigen: Human Apolipoprotein AII Purification: Affinity purified Form: Freeze dried powder Buffer: 75 mM Sodium Phosphate, 75 mM NaCl, 0.5 mM EDTA, 0.02% NaN3, pH 7.2 Specificity Specifically binds to human apo AII. Dilution for immunoblot and ELISA range:
mutant L343V and R463W altered folding of the alpha-helical domain within the N terminus of apoB (proper folding of the -helical domain within the N terminus of apoB is important for efficient secretion of apoB-containing lipoproteins ...
Elisha Cuthbert @ TRL Canuck cutie Elisha Cuthbert shows off her hockey skills on TRL from its Times Square studios in NYC on Thursday (taped on Monday). The actress has been promoting…
Navigation Data (b-13-72-np.050 [SINS]) YYYYMMDDHHMMSST YYYYMMDDHHMMSST 197207300820000 197209150119000 197209150519000 197209151245000 197209151310000 197209151310000 197209152044000 197209160920000 197209161354000 197209161354000 197209161415000 197209170134000 197209170540000 197209222345000 197209230022000 197209230022000 197209230116000 197209230116000 197209230208000 197209230208000 197209230330000 197209230330000 197209230540000 197209230600000 YYYYMMDDHHMMSST YYYYMMDDHHMMSST Magnetics Data (b-13-72-np.221_050) YYYYMMDDHHMMSST YYYYMMDDHHMMSST 197207302000000 197207310445000 197207310500000 197207310510000 197207310630000 197208011525000 197208020105000 197208020400000 197208020435000 197208021355000 197208022300000 197208031840000 197208040135000 197208040400000 197208040415000 197208040645000 197208040820000 197208041815000 197208050130000 197208051540000 197208060615000 197208060800000 197208060825000 197208061300000 197208061310000 197208062115000 197208070430000 197208070800000 ...
Vogelgesang S, Schroeder E, Walker LC, Pahnke J, Naubereit A, Walther R, Stausske D, Warzok RW. Activated microglia do not mediate the early deposition of Abeta in carriers of the apolipoprotein Eepsilon4 allele ...
This Histri was built automatically but not manually verified. As a consequence, the Histri can be incomplete or can contain errors ...
This Histri was built automatically but not manually verified. As a consequence, the Histri can be incomplete or can contain errors ...
To evaluate possible mechanisms by which insulin inhibits hepatic apolipoprotein B (apoB) secretion, we incubated primary cultures of rat hepatocytes with sodium ort ho vanadate, a phosphotyrosine phosphatase inhibitor and insulin-mimetic agent. Vanadate (10 μM) and insulin (10 nM) inhibited the medium accumulation of apoB (secretion) by 21 and 37%, respectively, without increasing intracellular apoB. The effects of insulin and vanadate together were not additive. Both insulin and vanadate enhanced intracellular glycogen accumulation by 82 and 37%, respectively. Unlike insulin, vanadate, at a concentration that inhibited apoB secretion (10 μM), had no effect on intracellular lipogenesis, inhibited the secretion of newly synthesized hepatic proteins, and had a delayed onset and termination of action on inhibition of apoB secretion. At higher concentrations (40 and 80 μM), vanadate stimulated intracellular lipogenesis. In conclusion, our data indicate that vanadate mimics insulin action in ...
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CONTENT: To assess the comparability of apo B and LDL-P, we reviewed 25 clinical studies containing 85 outcomes for which both biomarkers were determined. In 21 of 25 (84.0%) studies, both apo B and LDL-P were significant for at least 1 outcome. Neither was significant for any outcome in only 1 study (4.0%). In 50 of 85 comparisons (58.8%), both apo B and LDL-P had statistically significant associations with the clinical outcome, whereas in 17 comparisons (20.0%) neither was significantly associated with the outcome. In 18 comparisons (21.1%) there was discordance between apo B and LDL-P ...
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Niacin and niacinamide are indicated for prevention and treatment of vitamin B3 deficiency states. Vitamin B3 (Niacin) also acts to reduce LDL cholesterol, triglycerides, and HDL cholesterol. The magnitude of individual lipid and lipoprotein responses may be influenced by the severity and type of underlying lipid abnormality. The increase in total HDL is associated with a shift in the distribution of HDL subfractions (as defined by ultra-centrifugation) with an increase in the HDL2:HDL3 ratio and an increase in apolipoprotein A-I content. Vitamin B3 (Niacin) treatment also decreases the serum levels of apolipoprotein B-100 (apo B), the major protein component of the VLDL (very low-density lipoprotein) and LDL fractions, and of lipoprotein-a, a variant form of LDL independently associated with coronary risk ...
Niacin and niacinamide are indicated for prevention and treatment of vitamin B3 deficiency states. Vitamin B3 (Niacin) also acts to reduce LDL cholesterol, triglycerides, and HDL cholesterol. The magnitude of individual lipid and lipoprotein responses may be influenced by the severity and type of underlying lipid abnormality. The increase in total HDL is associated with a shift in the distribution of HDL subfractions (as defined by ultra-centrifugation) with an increase in the HDL2:HDL3 ratio and an increase in apolipoprotein A-I content. Vitamin B3 (Niacin) treatment also decreases the serum levels of apolipoprotein B-100 (apo B), the major protein component of the VLDL (very low-density lipoprotein) and LDL fractions, and of lipoprotein-a, a variant form of LDL independently associated with coronary risk ...
We have previously reported a positive correlation between the expression of BHMT (betaine-homocysteine S-methyltransferase) and ApoB (apolipoprotein B) in rat hepatoma McA (McArdle RH-7777) cells [Sowden, Collins, Smith, Garrow, Sparks and Sparks (1999) Biochem. J. 341, 639-645]. To examine whether a similar relationship occurs in vivo, hepatic BHMT expression was induced by feeding rats a Met (L-methionine)-restricted betaine-containing diet, and parameters of ApoB metabolism were evaluated. There were no generalized metabolic abnormalities associated with Met restriction for 7 days, as evidenced by control levels of serum glucose, ketones, alanine aminotransferase and L-homocysteine levels. Betaine plus the Met restriction resulted in lower serum insulin and non-esterified fatty acid levels. Betaine plus Met restriction induced hepatic BHMT 4-fold and ApoB mRNA 3-fold compared with Met restriction alone. No changes in percentage of edited ApoB mRNA were observed on the test diets. An increase ...
Human genetic research can pinpoint drug targets by identifying complete loss-of-function mutations affecting a human gene product that, in turn, underlie a favorable phenotype.1 Most small-molecule oral drugs, monoclonal antibodies, or RNA-based strategies act by inhibiting a selected molecular target, thereby pharmacologically mimicking the naturally advantageous genetic deficiency. The fields of atherosclerosis and lipoprotein biology have several examples of drugs whose raison dêtre is to impersonate a naturally occurring, genetically determined beneficial phenotype.. Article see p 677. For instance, 3 new classes of agents approved in the United States reduce low-density lipoprotein (LDL)-cholesterol levels through nonstatin mechanisms.2,3 These include (1) an oral inhibitor of microsomal triglyceride transfer protein (MTP), namely lomitapide (Juxtapid; Aegerion); (2) an injectable antisense oligonucleotide against apolipoprotein (apo) B, namely mipomersen (Kynamro; ISIS-Genzyme); and (3) ...
A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of Low-Density Lipoproteins (Lipoproteins, LDL; Lipoproteins, VLDL). It is the ligand for the LDL Receptor (Receptors, LDL) that promotes cellular binding and internalization of LDL particles ...
Homo sapiens apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3D (putative) (APOBEC3D), mRNA. (H00140564-R01) - Products - Abnova
Cardiology news, research and treatment articles offering cardiology healthcare professionals cardiology information and resources to keep them informed.
This test measures the amount of a protein in your blood related to LDL and HDL cholesterol. It can help predict your risk for heart disease.
This test measures the amount of a protein in your blood related to LDL and HDL cholesterol. It can help predict your risk for heart disease.
Definition of TRL in the Financial Dictionary - by Free online English dictionary and encyclopedia. What is TRL? Meaning of TRL as a finance term. What does TRL mean in finance?
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An elevated plasma level of apolipoprotein B (apoB), the major protein of low density lipoproteins, is a risk factor for coronary artery disease. This study tested the hypothesis, suggested by previous studies, that the apoB level is strongly influenced by a major gene. The study population included 832 family members of 116 subjects who had undergone elective coronary arteriography at an early age. The apoB level was adjusted for age, gender, body mass index, alcohol consumption, and cigarette smoking (R2 = 20 %). ApoB levels revealed strong familial aggregation with correlations among spouses of 0.23, parent-offspring of 0.16, and siblings of 0.21. Regressive models were used to examine inter-individual variation in adjusted apoB levels. In the total sample, familial aggregation of the apoB level was consistent with two models: (1) a major gene model and (2) a polygenic model with a mixture of non-transmitted "types." Comparison of these two models in each family showed that 57 families ...
We have reported studies characterizing small-molecule inhibitors that selectively inhibit PLTP activity and concomitantly reduce apoB secretion. In the present study, we identified small molecules that inhibit both PLTP and MTP activities, which are known to regulate apoB secretion. This is the first report to identify dual inhibitors for PLTP and MTP activities. The discovery was not expected based on the lack of homology of PLTP and MTP at protein sequence levels. Although CETP and PLTP have 40% homology and belong to the family of lipid transfer/lipopolysaccharide-binding proteins (Tollefson et al., 1988; Day et al., 1994), none of these compounds inhibit CETP activity (Luo et al., 2010). MTP and apoB belong to the vitellogenin family of lipid transfer proteins. Read et al. (2000) predicted the three-dimensional structure of the C-terminal lipid binding cavity of MTP based on the crystal structure of lipoviellin. The lipid cavity in MTP bears a resemblance to the lipid binding domain of ...
Macrophage receptor that binds to the apolipoprotein B48 (APOB) of dietary triglyceride (TG)-rich lipoproteins (TRL) or to a like domain of APOB in hypertriglyceridemic very low density lipoprotein (HTG-VLDL). Binds and internalizes TRL when out of the context of the macrophage. May provide essential lipids to reticuloendothelial cells. Could also be involved in foam cell formation with elevated TRL and remnant lipoprotein (RLP). Mediates the rapid high-affinity uptake of chylomicrons (CM), HTG-VLDL, and trypsinized (tryp) VLDL devoid of APOE in vitro in macrophages.
The sine qua non of atherosclerosis is the presence of sterols in arterial wall macrophages. Sterols are delivered to the arterial wall by the penetration of the endothelium by an apoB-containing lipoprotein, which transport the sterols. In other words, unless an apoB-containing lipoprotein particle violates the border created by an endothelium cell and the layer it protects, the media layer, there is no way atherogenesis occurs. For now, lets focus only on the most ubiquitous apoB-containing lipoprotein, the LDL particle. Yes, other lipoproteins also contain apoB (e.g., chylomicrons, remnant lipoproteins such as VLDL remnants, IDL and Lp(a)), but they are few in number relative to LDL particles. I will address them later.. The endothelium is the one-cell-thick-layer which lines the lumen (i.e., the "tube") of a vessel, in this case, the artery. Since blood is in direct contact with this cell all the time, all lipoproteins - including LDL particles - come in constant contact with such ...
Looking for online definition of atherogenicity in the Medical Dictionary? atherogenicity explanation free. What is atherogenicity? Meaning of atherogenicity medical term. What does atherogenicity mean?

Native Human Apolipoprotein C-I Protein |  Cell SciencesNative Human Apolipoprotein C-I Protein | Cell Sciences

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Apolipoprotein C-II deficiency (APOC2) DNA Test Lab Cost INR 30000.00 best genetic offer discount price Delhi Mumbai Kolkata...Apolipoprotein C-II deficiency (APOC2) DNA Test Lab Cost INR 30000.00 best genetic offer discount price Delhi Mumbai Kolkata...

Apolipoprotein C-II deficiency (APOC2) Test Cost INR 30000.00 Surat Pune Jaipur Lucknow Kanpur Nagpur Visakhapatnam Indore ... Apolipoprotein C-II deficiency (APOC2) Test Description. Apolipoprotein C-II deficiency (APOC2) Apolipoprotein C-II deficiency ... Apolipoprotein C-II deficiency (APOC2) TEST DETAILS. Deatils about the test Apolipoprotein C-II deficiency (APOC2). *What is ... Make the payment Online for Apolipoprotein C-II deficiency (APOC2). * Fill the Form with your details for Apolipoprotein C-II ...
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Apob - Apolipoprotein B-100 precursor - Mus musculus (Mouse) - Apob gene & proteinApob - Apolipoprotein B-100 precursor - Mus musculus (Mouse) - Apob gene & protein

Apolipoprotein B is a major protein constituent of chylomicrons (apo B-48), LDL (apo B-100) and VLDL (apo B-100). Apo B-100 ... Apolipoprotein B-48Add BLAST. 2151. Amino acid modifications. Feature key. Position(s). DescriptionActions. Graphical view. ... Apolipoprotein B is a major protein constituent of chylomicrons (apo B-48), LDL (apo B-100) and VLDL (apo B-100). Apo B-100 ... sp,E9Q414,APOB_MOUSE Apolipoprotein B-100 OS=Mus musculus OX=10090 GN=Apob PE=1 SV=1 ...
more infohttps://www.uniprot.org/uniprot/E9Q414

Apob - Apolipoprotein B-100 precursor - Rattus norvegicus (Rat) - Apob gene & proteinApob - Apolipoprotein B-100 precursor - Rattus norvegicus (Rat) - Apob gene & protein

Apolipoprotein B is a major protein constituent of chylomicrons (apo B-48), LDL (apo B-100) and VLDL (apo B-100). Apo B-100 ... Apolipoprotein B-48Add BLAST. 2119. Amino acid modifications. Feature key. Position(s). DescriptionActions. Graphical view. ... Apolipoprotein B-100Add BLAST. 4716. ,p>This subsection of the PTM / Processing section describes the extent of a polypeptide ... "Identification of circulating apolipoproteins synthesized by rat small intestine in vivo.". Wu A.L., Windmueller H.G.. J. Biol ...
more infohttp://www.uniprot.org/uniprot/Q7TMA5

Defective Apolipoprotein B-100Defective Apolipoprotein B-100

The terms "Defective Apolipoprotein B-100" returned 27 free, full-text research articles on human participants. First 3 results ... Familial defective apolipoprotein B-100 is a genetic disorder of apolipoprotein B-100 that causes moderate to severe ... A single amino acid mutation in apolipoprotein B diminishes the ability of low density lipoproteins to bind to the low density ... Familial defective apolipoprotein B-100 and increased low-density lipoprotein cholesterol and coronary artery calcification in ...
more infohttp://diseaseinfosearch.org/Defective+Apolipoprotein+B-100/2166

Recombinant Human Antibodies Against Aldehyde-Modified Apolipoprotein B-100 Peptide Sequences Inhibit Atherosclerosis |...Recombinant Human Antibodies Against Aldehyde-Modified Apolipoprotein B-100 Peptide Sequences Inhibit Atherosclerosis |...

Developmental and age-related changes in apolipoprotein B mRNA editing in mice. J Lipid Res. 1992; 33: 1753-1764. ... Recombinant Human Antibodies Against Aldehyde-Modified Apolipoprotein B-100 Peptide Sequences Inhibit Atherosclerosis. ... Aldehyde-modified peptide sequences in apolipoprotein B-100 (apoB-100) are major targets for these immune responses. ... Recombinant Human Antibodies Against Aldehyde-Modified Apolipoprotein B-100 Peptide Sequences Inhibit Atherosclerosis ...
more infohttp://circ.ahajournals.org/content/110/14/2047

S07] Goat Anti-Human Apolipoprotein B-100 Antiserum - AcademyBiomedS07] Goat Anti-Human Apolipoprotein B-100 Antiserum - AcademyBiomed

Use: The antibody can be used for detection of apo B-100 in plasma and lipoproteins, immunoassays, immunoblots, enzyme ... Human Apolipoprotein B100 Specificity Specifically binds to human apo B-100. Dilution for immunoblot and ELISA range: 1,000 to ... Human Apolipoprotein B100. Specificity. Specifically binds to human apo B-100. Dilution for immunoblot and ELISA range: 1,000 ... "Apolipoprotein B-48 Is the Product of a Messenger RNA with an Organ-specific In-frame Stop Codon." Science 238 (1987): 363- 66. ...
more infohttps://www.academybiomed.com/products/s07-goat-anti-human-apolipoprotein-b-100-antiserum

Immunotherapy With Tolerogenic Apolipoprotein B-100-Loaded Dendritic Cells Attenuates Atherosclerosis in Hypercholesterolemic...Immunotherapy With Tolerogenic Apolipoprotein B-100-Loaded Dendritic Cells Attenuates Atherosclerosis in Hypercholesterolemic...

Immunotherapy With Tolerogenic Apolipoprotein B-100-Loaded Dendritic Cells Attenuates Atherosclerosis in Hypercholesterolemic ... Immunotherapy With Tolerogenic Apolipoprotein B-100-Loaded Dendritic Cells Attenuates Atherosclerosis in Hypercholesterolemic ... Immunotherapy With Tolerogenic Apolipoprotein B-100-Loaded Dendritic Cells Attenuates Atherosclerosis in Hypercholesterolemic ... Immunotherapy With Tolerogenic Apolipoprotein B-100-Loaded Dendritic Cells Attenuates Atherosclerosis in Hypercholesterolemic ...
more infohttp://circ.ahajournals.org/content/early/2011/02/28/CIRCULATIONAHA.110.973222

Apolipoprotein B-100 (Apo B-100), Human Pl | LeeBio.comApolipoprotein B-100 (Apo B-100), Human Pl | LeeBio.com

Buy high purity human plasma Apolipoprotein B (APO B-100) antigen for research, life science and diagnostic manufacturing uses ... 125-25 - Apolipoprotein B from human plasma - >80% (SDS-PAGE). 125-26 - Goat anti-Human Apolipoprotein B Polyclonal Antibody. ... Buy Human Apolipoprotein B-100 (ApoB-100) from Lee Biosolutions. Custom preparations, technical support, bulk quantities and ...
more infohttps://www.leebio.com/product/654/apolipoprotein-b-100-apo-b-100-human-plasma-125-18

Estrogen-enhanced apical and basolateral secretion of apolipoprotein B-100 by polarized trophoblast-derived BeWo cells.Estrogen-enhanced apical and basolateral secretion of apolipoprotein B-100 by polarized trophoblast-derived BeWo cells.

... ... Das Ziel dieser Arbeit war es, die Sekretion von Apolipoprotein B 100 (ApoB) - enthaltenden Lipoproteinen an der basalen Seite ... Zusätzlich wurde die plazentare Lokalisation von Apolipoprotein-Rezeptoren (LRP2, LDLR, LRP1) untersucht, um zelluläre Ziele ...
more infohttps://www.meduniwien.ac.at/hp/ipa/research-news/single-view/?tx_ttnews%5Btt_news%5D=4353&cHash=0fb49127763478ee7573516fcb8af672

Familial defective apolipoprotein B-100 - RightDiagnosis.comFamilial defective apolipoprotein B-100 - RightDiagnosis.com

Defective apolipoprotein B-100) with alternative diagnoses, full-text book chapters, misdiagnosis, research treatments, ... and treatment information for Familial defective apolipoprotein B-100 ( ... Apolipoprotein B *Familial *Familial disorder *Defective *Apolipoprotein Familial defective apolipoprotein B-100 as a Disease. ... OMIM - APOLIPOPROTEIN B; APOB Source: Diseases Database Interesting Medical Articles:. *Symptoms of the Silent Killer Diseases ...
more infohttps://www.rightdiagnosis.com/medical/familial_defective_apolipoprotein_b_100.htm

Monogenic hypercholesterolemia in South Africans : familial hypercholesterolemia in Indians and familial defective...Monogenic hypercholesterolemia in South Africans : familial hypercholesterolemia in Indians and familial defective...

... familial hypercholesterolemia in Indians and familial defective apolipoprotein B-100. [David Chaim Rubinsztein] ... Apolipoproteins B a schema:Intangible ;. schema:name "Apolipoproteins B"@en ;. . ... schema:about apolipoproteins_b> ; # Apolipoproteins B schema: ... familial hypercholesterolemia in Indians and familial defective apolipoprotein B-100. Author:. David Chaim Rubinsztein. ...
more infohttp://www.worldcat.org/title/monogenic-hypercholesterolemia-in-south-africans-familial-hypercholesterolemia-in-indians-and-familial-defective-apolipoprotein-b-100/oclc/890418932

Intranasal Immunization With an Apolipoprotein B-100 Fusion Protein Induces Antigen-Specific Regulatory T Cells and Reduces...Intranasal Immunization With an Apolipoprotein B-100 Fusion Protein Induces Antigen-Specific Regulatory T Cells and Reduces...

Tenger C, Zhou X. Apolipoprotein e modulates immune activation by acting on the antigen-presenting cell. Immunology. 2003; 109 ... A peptide sequence from apolipoprotein B-100 of low-density lipoprotein was fused with the B subunit of cholera toxin and used ... Intranasal Immunization With an Apolipoprotein B-100 Fusion Protein Induces Antigen-Specific Regulatory T Cells and Reduces ... Intranasal Immunization With an Apolipoprotein B-100 Fusion Protein Induces Antigen-Specific Regulatory T Cells and Reduces ...
more infohttp://atvb.ahajournals.org/content/30/5/946.long

Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics |...Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics |...

Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics. ... Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics ... Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics ... Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics ...
more infohttp://atvb.ahajournals.org/content/26/3/590

Cholesterol Substrate Availability as a Regulator of the Hepatic Secretion Rate of Very-Low-Density Lipoprotein Apolipoprotein...Cholesterol Substrate Availability as a Regulator of the Hepatic Secretion Rate of Very-Low-Density Lipoprotein Apolipoprotein...

Cholesterol Substrate Availability as a Regulator of the Hepatic Secretion Rate of Very-Low-Density Lipoprotein Apolipoprotein ... Cholesterol Substrate Availability as a Regulator of the Hepatic Secretion Rate of Very-Low-Density Lipoprotein Apolipoprotein ... Cholesterol Substrate Availability as a Regulator of the Hepatic Secretion Rate of Very-Low-Density Lipoprotein Apolipoprotein ... Cholesterol Substrate Availability as a Regulator of the Hepatic Secretion Rate of Very-Low-Density Lipoprotein Apolipoprotein ...
more infohttp://www.clinsci.org/content/89/s33/15P.3

Familial defective apolipoprotein B-100 in 12 subjects and their kindredFamilial defective apolipoprotein B-100 in 12 subjects and their kindred

... Geisel J, Schleifenbaum T, Oette K, Weisshaar B (1992 ... Familial defective apolipoprotein B-100 in 12 subjects and their kindred. European Journal of Clinical Chemistry and Clinical ... "Familial defective apolipoprotein B-100 in 12 subjects and their kindred". European Journal of Clinical Chemistry and Clinical ... Familial ligand-defective apolipoprotein B. Identification of a new mutation that decreases LDL receptor binding affinity.. ...
more infohttps://pub.uni-bielefeld.de/publication/1868003

Association of DNA Polymorphism at the Apolipoprotein B-100 Gene Locus with Plasma Lipid Concentration and Coronary Artery...Association of DNA Polymorphism at the Apolipoprotein B-100 Gene Locus with Plasma Lipid Concentration and Coronary Artery...

LDL-cholesterol and Apolipoprotein B levels. The study elucidates that ApoB gene polymorphisms are associated with CAD in north ... The aim of this study was to investigate the association between apolipoprotein B gene polymorphisms and coronary artery ... The aim of this study was to investigate the association between apolipoprotein B gene polymorphisms and coronary artery ... Association of DNA Polymorphism at the Apolipoprotein B-100 Gene Locus with Plasma Lipid Concentration and Coronary Artery ...
more infohttps://thescipub.com/abstract/10.3844/ajbbsp.2006.138.145

Improved detection of familial defective apolipoprotein B-100 by restriction-site-introducing polymerase chain reactionImproved detection of familial defective apolipoprotein B-100 by restriction-site-introducing polymerase chain reaction

Familial defective apolipoprotein B-100 homozygote with premature coronary atherosclerosis. A case report.. Horinek A, Ceska R ... Improved detection of familial defective apolipoprotein B-100 by restriction-site-introducing polymerase chain reaction. Geisel ... Geisel J, Schleifenbaum T, Weisshaar B, Oette K. Improved detection of familial defective apolipoprotein B-100 by restriction- ... Geisel, J., Schleifenbaum, T., Weisshaar, B., and Oette, K. (1993). Improved detection of familial defective apolipoprotein B- ...
more infohttps://pub.uni-bielefeld.de/publication/1867989

Human placenta secretes apolipoprotein B-100-containing lipoproteinsHuman placenta secretes apolipoprotein B-100-containing lipoproteins

Forskning , Publikationer , Human placenta secretes apolipoprotein B-100-containing lipoproteins Human placenta secretes ... In mice, disruption of yolk sac cell secretion of apolipoprotein (apo) B-containing lipoproteins results in embryonic lethality ... 35)S-labeled apoB-100 was recovered in d approximately 1.02-1.04 g/ml particles (i.e. similar to the density of plasma low ... These results demonstrate that human placenta expresses both apoB and MTP and consequently synthesize and secrete apoB-100- ...
more infohttps://curis.ku.dk/portal/da/publications/human-placenta-secretes-apolipoprotein-b100containing-lipoproteins

Decreased bone mineral density in subjects carrying familial defective apolipoprotein B-100.  - PubMed - NCBIDecreased bone mineral density in subjects carrying familial defective apolipoprotein B-100. - PubMed - NCBI

Decreased bone mineral density in subjects carrying familial defective apolipoprotein B-100.. Yerges-Armstrong LM1, Shen H, ... Defective Apolipoprotein B-100 - Genetic Alliance. Molecular Biology Databases. *Pharmacogenomic Annotation 15065754 for PMID: ... Decreased Bone Mineral Density in Subjects Carrying Familial Defective Apolipoprotein B-100 ... the cause of familial defective apolipoprotein B-100, which has been previously shown to markedly increase low-density ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=87638

Defective apolipoprotein B-100             | Genetic and Rare Diseases Information Center (GARD) - an NCATS ProgramDefective apolipoprotein B-100 | Genetic and Rare Diseases Information Center (GARD) - an NCATS Program

... resources and questions answered by our Genetic and Rare Diseases Information Specialists for Defective apolipoprotein B-100 ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=cluster&id=24522

Metabolism of apolipoprotein B-100-containing lipoproteins in dyslipidaemias<...Metabolism of apolipoprotein B-100-containing lipoproteins in dyslipidaemias<...

Metabolism of apolipoprotein B-100-containing lipoproteins in dyslipidaemias. / Watts, Gerald; Chan, Doris; Barrett, Hugh. ... Metabolism of apolipoprotein B-100-containing lipoproteins in dyslipidaemias. Gerald Watts, Doris Chan, Hugh Barrett ... Watts, G., Chan, D., & Barrett, H. (2007). Metabolism of apolipoprotein B-100-containing lipoproteins in dyslipidaemias. In C. ... Metabolism of apolipoprotein B-100-containing lipoproteins in dyslipidaemias. The Year in Lipid Disorders. editor / C.J. ...
more infohttps://research-repository.uwa.edu.au/en/publications/metabolism-of-apolipoprotein-b-100-containing-lipoproteins-in-dys

Apolipoprotein B100 - AHealthyMe - Blue Cross Blue Shield of MassachusettsApolipoprotein B100 - AHealthyMe - Blue Cross Blue Shield of Massachusetts

ApoB100, Apolipoprotein B, ApoB, Apolipoprotein (B). What is this test?. This test measures the amount of a certain type of ... Apolipoprotein B-100. Does this test have other names?. ... cholesterol called apolipoprotein B-100 (ApoB) in your blood. ... Results are given in milligrams per deciliter (mg/dL). Normal levels of Apo B-100 in adults are less than 100 mg/dL. Your risk ...
more infohttp://www.ahealthyme.com/Library/DiseasesConditions/Adult/Orthopedic/167,apolipoprotein_b100

Apolipoprotein B100 - AHealthyMe - Blue Cross Blue Shield of MassachusettsApolipoprotein B100 - AHealthyMe - Blue Cross Blue Shield of Massachusetts

ApoB100, Apolipoprotein B, ApoB, Apolipoprotein (B). What is this test?. This test measures the amount of a certain type of ... Apolipoprotein B-100. Does this test have other names?. ... cholesterol called apolipoprotein B-100 (ApoB) in your blood. ... Results are given in milligrams per deciliter (mg/dL). Normal levels of Apo B-100 in adults are less than 100 mg/dL. Your risk ...
more infohttp://www.ahealthyme.com/Library/DiseasesConditions/Adult/Women/167,apolipoprotein_b100

Attenuation of atherogenic apo B-48-dependent hyperlipidemia and high density lipoprotein remodeling induced by vitamin C and E...Attenuation of atherogenic apo B-48-dependent hyperlipidemia and high density lipoprotein remodeling induced by vitamin C and E...

... polyclonal anti-apolipoprotein A-I (apo A-I) (1:2000 dilution), and anti-apolipoprotein B-48 (apo B-48) (1:2000 dilution) ... d Apolipoprotein A-I abundance. e Phospholipid transfer protein (PLTP) activity. f PLTP abundance. Experimental data were ... Serum apolipoprotein B-100 (apo B-100) levels were measured using Mouse Apolipoprotein B (APOB) ELISA (Cusabio Biotech Co. Ltd ... b HDL apolipoprotein D abundance. c Antioxidant HDL capacity. Experimental data were collected from four independent animal ...
more infohttps://link.springer.com/article/10.1186%2Fs40659-018-0183-6
  • It comprises approximately half of the N-terminal region of ApoB-100 and is the result of posttranscriptional mRNA editing by a stop codon in the intestine not found in the liver. (academybiomed.com)
  • Zusätzlich wurde die plazentare Lokalisation von Apolipoprotein-Rezeptoren (LRP2, LDLR, LRP1) untersucht, um zelluläre Ziele und Aufnahmewege der Lipoproteinpartikel im plazentaren Gewebe zu identifizieren. (meduniwien.ac.at)
  • This effect was accompanied by induction of regulatory T cells that markedly suppressed effector T cells rechallenged with apoB-100 and increased numbers of interleukin (IL)-10 + CD4 + T cells. (ahajournals.org)
  • Apo B-100 is a large monomeric protein, containing 4536 amino acids (m.w. 515 kDa, Yang et al. (academybiomed.com)
  • C , Flow cytometry histogram of Nur77-GFP expression in splenic TRBV31 + CD3 + CD4 + T-helper cells 16 hours after injection (inj) of 100 μg LDL intraperitoneally, showing 1 representative experiment of 3. (nih.gov)
  • Apo B-100 is recognized by receptors found on the surface of many of the body's cells. (labtestsonline.org)