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.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.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.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 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.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).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.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-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.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 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.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.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: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.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.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.TriglyceridesLipoprotein(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.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.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.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)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.Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Cholesterol, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.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.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.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.Cholesterol, LDL: Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.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.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.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.Hyperlipidemias: Conditions with excess LIPIDS in the blood.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.Mice, Inbred C57BLLipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.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.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.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.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.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.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.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.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.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).Hypertriglyceridemia: A condition of elevated levels of TRIGLYCERIDES in the blood.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.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.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.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.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)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.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.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.Aorta: The main trunk of the systemic arteries.Diet, Atherogenic: A diet that contributes to the development and acceleration of ATHEROGENESIS.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.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.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.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Dietary 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.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Heterozygote: An individual having different alleles at one or more loci regarding a specific character.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.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.Dimyristoylphosphatidylcholine: A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.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.Cholesterol Ester Transfer Proteins: Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.Cytidine Deaminase: An enzyme that catalyzes the deamination of cytidine, forming uridine. EC 3.5.4.5.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.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.)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, Dietary: Cholesterol present in food, especially in animal products.Kinetics: The rate dynamics in chemical or physical systems.Aortic Diseases: Pathological processes involving any part of the AORTA.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.Particle Size: Relating to the size of solids.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.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).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.Gene Frequency: The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.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.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.Foam Cells: Lipid-laden macrophages originating from monocytes or from smooth muscle cells.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)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.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.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.LDL-Receptor Related Proteins: A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.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.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.Amyloidosis, Familial: Diseases in which there is a familial pattern of AMYLOIDOSIS.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)Serum Amyloid A Protein: An ACUTE PHASE REACTION protein present in low concentrations in normal sera, but found at higher concentrations in sera of older persons and in patients with AMYLOIDOSIS. It is the circulating precusor of amyloid A protein, which is found deposited in AA type AMYLOID FIBRILS.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.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Aryldialkylphosphatase: An enzyme which catalyzes the hydrolysis of an aryl-dialkyl phosphate to form dialkyl phosphate and an aryl alcohol. It can hydrolyze a broad spectrum of organophosphate substrates and a number of aromatic carboxylic acid esters. It may also mediate an enzymatic protection of LOW DENSITY LIPOPROTEINS against oxidative modification and the consequent series of events leading to ATHEROMA formation. The enzyme was previously regarded to be identical with Arylesterase (EC 3.1.1.2).Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Triolein: (Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.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.Amyloid beta-Peptides: Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.Scavenger Receptors, Class B: A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.Anticholesteremic Agents: Substances used to lower plasma CHOLESTEROL levels.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Time Factors: Elements of limited time intervals, contributing to particular results or situations.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.Hypolipidemic Agents: Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.Hyperlipoproteinemia Type V: A severe type of hyperlipidemia, sometimes familial, that is characterized by the elevation of both plasma CHYLOMICRONS and TRIGLYCERIDES contained in VERY-LOW-DENSITY LIPOPROTEINS. Type V hyperlipoproteinemia is often associated with DIABETES MELLITUS and is not caused by reduced LIPOPROTEIN LIPASE activity as in HYPERLIPOPROTEINEMIA TYPE I .Intestines: The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.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.Plaque, Atherosclerotic: Lesions formed within the walls of ARTERIES.Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Electrophoresis, Agar Gel: Electrophoresis in which agar or agarose gel is used as the diffusion medium.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.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)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).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.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.Protein Structure, Secondary: The level of protein structure in which regular hydrogen-bond interactions within contiguous stretches of polypeptide chain give rise to alpha helices, beta strands (which align to form beta sheets) or other types of coils. This is the first folding level of protein conformation.Postprandial Period: The time frame after a meal or FOOD INTAKE.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Lymph: The interstitial fluid that is in the LYMPHATIC SYSTEM.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.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.Protein Isoforms: Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.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.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.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.Brachiocephalic Trunk: The first and largest artery branching from the aortic arch. It distributes blood to the right side of the head and neck and to the right arm.Fenofibrate: An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.Lipocalins: A diverse family of extracellular proteins that bind to small hydrophobic molecules. They were originally characterized as transport proteins, however they may have additional roles such as taking part in the formation of macromolecular complexes with other proteins and binding to CELL SURFACE RECEPTORS.Phospholipid Transfer Proteins: A ubiquitous family of proteins that transport PHOSPHOLIPIDS such as PHOSPHATIDYLINOSITOL and PHOSPHATIDYLCHOLINE between membranes. They play an important role in phospholipid metabolism during vesicular transport and SIGNAL TRANSDUCTION.Chromatography, Gel: Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.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.Receptors, Scavenger: A large group of structurally diverse cell surface receptors that mediate endocytic uptake of modified LIPOPROTEINS. Scavenger receptors are expressed by MYELOID CELLS and some ENDOTHELIAL CELLS, and were originally characterized based on their ability to bind acetylated LOW-DENSITY LIPOPROTEINS. They can also bind a variety of other polyanionic ligand. Certain scavenger receptors can internalize micro-organisms as well as apoptotic cells.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).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.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.Antigens, CD36: Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.Genetic Variation: Genotypic differences observed among individuals in a population.Lecithin Acyltransferase Deficiency: An autosomal recessively inherited disorder caused by mutation of LECITHIN CHOLESTEROL ACYLTRANSFERASE that facilitates the esterification of lipoprotein cholesterol and subsequent removal from peripheral tissues to the liver. This defect results in low HDL-cholesterol level in blood and accumulation of free cholesterol in tissue leading to a triad of CORNEAL OPACITY, hemolytic anemia (ANEMIA, HEMOLYTIC), and PROTEINURIA.Fasting: Abstaining from all food.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.Macrophages, Peritoneal: Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.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.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.Oxidation-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).beta 2-Glycoprotein I: A 44-kDa highly glycosylated plasma protein that binds phospholipids including CARDIOLIPIN; APOLIPOPROTEIN E RECEPTOR; membrane phospholipids, and other anionic phospholipid-containing moieties. It plays a role in coagulation and apoptotic processes. Formerly known as apolipoprotein H, it is an autoantigen in patients with ANTIPHOSPHOLIPID ANTIBODIES.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.Probucol: A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).Brain: The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.Hyperlipoproteinemia Type I: An inherited condition due to a deficiency of either LIPOPROTEIN LIPASE or APOLIPOPROTEIN C-II (a lipase-activating protein). The lack of lipase activities results in inability to remove CHYLOMICRONS and TRIGLYCERIDES from the blood which has a creamy top layer after standing.Hepatocytes: The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.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.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.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)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.Sinus of Valsalva: The dilatation of the aortic wall behind each of the cusps of the aortic valve.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.Mice, Mutant Strains: Mice bearing mutant genes which are phenotypically expressed in the animals.Lipoproteins, HDL2: Low-density subclass of the high-density lipoproteins, with particle sizes between 8 to 13 nm.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Aging: The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.Peptides: Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.Haptoglobins: Plasma glycoproteins that form a stable complex with hemoglobin to aid the recycling of heme iron. They are encoded in man by a gene on the short arm of chromosome 16.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.Hydroxymethylglutaryl-CoA Reductase Inhibitors: Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.Amyloid: A fibrous protein complex that consists of proteins folded into a specific cross beta-pleated sheet structure. This fibrillar structure has been found as an alternative folding pattern for a variety of functional proteins. Deposits of amyloid in the form of AMYLOID PLAQUES are associated with a variety of degenerative diseases. The amyloid structure has also been found in a number of functional proteins that are unrelated to disease.Molecular Weight: The sum of the weight of all the atoms in a molecule.Esterification: The process of converting an acid into an alkyl or aryl derivative. Most frequently the process consists of the reaction of an acid with an alcohol in the presence of a trace of mineral acid as catalyst or the reaction of an acyl chloride with an alcohol. Esterification can also be accomplished by enzymatic processes.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.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.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Diet: Regular course of eating and drinking adopted by a person or animal.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.Hepatocyte Nuclear Factor 4: A subfamily of nuclear receptors that regulate GENETIC TRANSCRIPTION of a diverse group of GENES involved in the synthesis of BLOOD COAGULATION FACTORS; and in GLUCOSE; CHOLESTEROL; and FATTY ACIDS metabolism.Heptanoic Acids: 7-carbon saturated monocarboxylic acids.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.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.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.Promoter Regions, Genetic: DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.Cerebral Amyloid Angiopathy: A heterogeneous group of sporadic or familial disorders characterized by AMYLOID deposits in the walls of small and medium sized blood vessels of CEREBRAL CORTEX and MENINGES. Clinical features include multiple, small lobar CEREBRAL HEMORRHAGE; cerebral ischemia (BRAIN ISCHEMIA); and CEREBRAL INFARCTION. Cerebral amyloid angiopathy is unrelated to generalized AMYLOIDOSIS. Amyloidogenic peptides in this condition are nearly always the same ones found in ALZHEIMER DISEASE. (from Kumar: Robbins and Cotran: Pathologic Basis of Disease, 7th ed., 2005)Heparin: A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.Carotid Arteries: Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.Amyloidosis: A group of sporadic, familial and/or inherited, degenerative, and infectious disease processes, linked by the common theme of abnormal protein folding and deposition of AMYLOID. As the amyloid deposits enlarge they displace normal tissue structures, causing disruption of function. Various signs and symptoms depend on the location and size of the deposits.Vascular Cell Adhesion Molecule-1: Cytokine-induced cell adhesion molecule present on activated endothelial cells, tissue macrophages, dendritic cells, bone marrow fibroblasts, myoblasts, and myotubes. It is important for the recruitment of leukocytes to sites of inflammation. (From Pigott & Power, The Adhesion Molecule FactsBook, 1993, p154)Aorta, Thoracic: The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.Electrophoresis, Gel, Two-Dimensional: Electrophoresis in which a second perpendicular electrophoretic transport is performed on the separate components resulting from the first electrophoresis. This technique is usually performed on polyacrylamide gels.Liposomes: Artificial, single or multilaminar vesicles (made from lecithins or other lipids) that are used for the delivery of a variety of biological molecules or molecular complexes to cells, for example, drug delivery and gene transfer. They are also used to study membranes and membrane proteins.Chromatography, Affinity: A chromatographic technique that utilizes the ability of biological molecules to bind to certain ligands specifically and reversibly. It is used in protein biochemistry. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor.

Vitamin A is linked to the expression of the AI-CIII-AIV gene cluster in familial combined hyperlipidemia. (1/471)

There is growing evidence of the capacity of vitamin A to regulate the expression of the genetic region that encodes apolipoproteins (apo) A-I, C-III, and A-IV. This region in turn has been proposed to modulate the expression of hyperlipidemia in the commonest genetic form of dyslipidemia, familial combined hyperlipidemia (FCHL). The hypothesis tested here was whether vitamin A (retinol), by controlling the expression of the AI-CIII-AIV gene cluster, plays a role in modulating the hyperlipidemic phenotype in FCHL. We approached the subject by studying three genetic variants of this region: a C1100-T transition in exon 3 of the apoC-III gene, a G3206-T transversion in exon 4 of the apoC-III gene, and a G-75-A substitution in the promoter region of the apoA-I gene. The association between plasma vitamin A concentrations and differences in the plasma concentrations of apolipoproteins A-I and C-III based on the different genotypes was assessed in 48 FCHL patients and 74 of their normolipidemic relatives. The results indicated that the subjects carrying genetic variants associated with increased concentrations of apoA-I and C-III (C1100-T and G-75-A) also presented increased plasma concentrations of vitamin A. This was only observed among the FCHL patients, which suggested that certain characteristics of these patients contributed to this association. The G3206-T was not associated with changes in either apolipoprotein concentrations or in vitamin A. In summary, we report a relationship between genetically determined elevations of proteins of the AI-CIII-AIV gene cluster and vitamin A in FCHL patients. More studies will be needed to confirm that vitamin A plays a role in FCHL which might also be important for its potential application to therapeutical approaches.  (+info)

Apolipoprotein A-I charge and conformation regulate the clearance of reconstituted high density lipoprotein in vivo. (2/471)

While low apolipoprotein A-I (apoA-I) levels are primarily associated with increased high density lipoprotein (HDL) fractional catabolic rate (FCR), the factors that regulate the clearance of HDL from the plasma are unclear. In this study, the effect of lipid composition of reconstituted HDL particles (LpA-I) on their rate of clearance from rabbit plasma has been investigated. Sonicated LpA-I containing 1 to 2 molecules of purified human apoA-I and 5 to 120 molecules of palmitoyl-oleoyl phosphatidylcholine (POPC) exhibit similar charge and plasma FCR to that for lipid free apoA-I, 2.8 pools/day. Inclusion of 1 molecule of apoA-II to an LpA-I complex increases the FCR to 3.5 pools/day, a value similar to that observed for exchanged-labeled HDL3. In contrast, addition of 40 molecules of triglyceride, diglyceride, or cholesteryl ester to a sonicated LpA-I containing 120 moles of POPC and 2 molecules of apoA-I increases the negative charge of the particle and reduces the FCR to 1.8 pools/day. Discoidal LpA-I are the most positively charged lipoprotein particles and also have the fastest clearance rates, 4.5 pools/day. Immunochemical characterization of the different LpA-I particles shows that the exposure of an epitope at residues 98 to 121 of the apoA-I molecule is associated with an increased negative particle charge and a slower clearance from the plasma. We conclude that the charge and conformation of apoA-I are sensitive to the lipid composition of LpA-I and play a central role in regulating the clearance of these lipoproteins from plasma. conformation regulate the clearance of reconstituted high density lipoprotein in vivo.  (+info)

Dietary restriction of saturated fat and cholesterol decreases HDL ApoA-I secretion. (3/471)

We examined the mechanisms responsible for the decrease in HDL cholesterol (HDL-C) levels after the consumption of a diet low in total fat, saturated fat, and cholesterol. Twenty-one subjects with a mean age of 58+/-12 years were placed on a baseline isocaloric diet (15% protein, 49% carbohydrate, 36% fat, and 150 mg/1000 kcals of cholesterol) and then switched to an NCEP Step 2 diet (15% protein, 60% carbohydrate, 25% fat, and 45 mg/1000 kcals of cholesterol). After 6 or 24 weeks on each diet, subjects received a 15-hour primed-constant infusion of [5,5,5-2H3]-L-leucine. HDL apoA-I and apoA-II tracer curves were determined by gas chromatography-mass spectrometry and fitted to a monoexponential equation. Compared with the baseline diet, consumption of the Step 2 diet lowered HDL-C mean levels by 15% (1.03+/-0.23 to 0.88+/-0.16 mmol/L, P<0.001), apoA-I by 12% (1.25+/-0.15 to 1.10+/-0.13 g/L, P<0. 001) and the TC/HDL-C ratio by 5% (0.145+/-0.04 to 0.137+/-0.03). No significant changes were observed in apoA-II levels and HDL particle size with diet. HDL apoA-I fractional catabolic rate did not change (0.219+/-0.052 to 0.220+/-0.043 pools/day, P=0.91) but HDL apoA-I secretion rate decreased by 8% (12.26+/-3.07 to 10.84+/-2.11 mg. kg-1. day-1, P=0.03) during consumption of the Step 2 diet. There was no effect of diet on apoA-II fractional catabolic rate or secretion rate. Our results indicate that the decrease in HDL-C and apoA-I levels during the isocaloric consumption of a Step 2 diet paralleled the reductions in apoA-I secretion rate.  (+info)

Acute effects of intravenous infusion of ApoA1/phosphatidylcholine discs on plasma lipoproteins in humans. (4/471)

To investigate the metabolism of nascent HDLs, apoA1/phosphatidylcholine (apoA1/PC) discs were infused IV over 4 hours into 7 healthy men. Plasma total apoA1 and phospholipid (PL) concentrations increased during the infusions. The rise in plasma apoA1 was greatest in small prebeta-migrating particles not present in the infusate. Total HDL unesterified cholesterol (UC) also increased simultaneously. After stopping the infusion, the concentrations of apoA1, PL, HDL UC, and small prebeta HDLs decreased, whereas those of HDL cholesteryl ester (CE) and large alpha-migrating apoA1 containing HDLs increased. ApoB-containing lipoproteins became enriched in CEs. Addition of apoA1/PC discs to whole blood at 37 degrees C in vitro also generated small prebeta HDLs, but did not augment the transfer of UC from erythrocytes to plasma. We conclude that the disc infusions increased the intravascular production of small prebeta HDLs in vivo, and that this was associated with an increase in the efflux and esterification of UC derived from fixed tissues. The extent to which the increase in tissue cholesterol efflux was dependent on that in prebeta HDL production could not be determined. Infusion of discs also reduced the plasma apoB and apoA2 concentrations, and increased plasma triglycerides and apoC3. Thus, nascent HDL secretion may have a significant impact on prebeta HDL production, reverse cholesterol transport and lipoprotein metabolism in humans.  (+info)

Apolipoprotein B-containing lipoproteins in renal failure: the relation to mode of dialysis. (5/471)

BACKGROUND: The aim of this study was to establish whether there is a differential effect of mode of dialysis, hemodialysis (HD), or continuous ambulatory peritoneal dialysis (CAPD) on the dyslipidemia of renal failure. METHODS: The lipoprotein profile was determined in 61 non-diabetic patients on chronic HD (N = 30) and CAPD treatment (N = 31), and in a control group of 27 healthy subjects. The analysis included the measurement of individual apolipoprotein (apo) A- and apo B-containing lipoproteins (LPs) separated by sequential immunoaffinity chromatography. Apo A-containing lipoproteins include lipoprotein A-I with apo A-I and lipoprotein A-I:A-II with apo A-I and apo A-II as the main protein constituents, whereas apo B-containing lipoproteins comprise simple cholesterol-rich lipoprotein B (LP-B), with apo B as the only protein moiety and complex triglyceride (TG)-rich lipoprotein B complex (LP-Bc) particles with apo B, apo A-II, apo C, and/or apo E as the protein constituents. RESULTS: CAPD patients had significantly higher concentrations of total cholesterol (6.8 vs. 5.1 mmol/liter), low-density lipoprotein (LDL) cholesterol (4.6 vs. 3.2 mmol/liter), TG (2.3 vs. 1.5 mmol/liter), apo B (155.3 vs. 105.7 mg/dl), LP-B (136.0 vs. 91.9 mg/dl), and LP-Bc (19.3 vs. 13.8 mg/dl) than HD patients. Both HD and CAPD patients had significantly higher TG, VLDL cholesterol, apo C-III, and apo E and significantly lower high-density lipoprotein cholesterol, apo A-II, and lipoprotein A-I:A-II levels than control subjects. The distribution of apo C-III in high-density lipoprotein and VLDL-LDL was altered in CAPD patients in comparison with control subjects. This suggests that the removal of TG-rich lipoproteins is less efficient in patients on CAPD. Normotriglyceridemic (NTG; TG < or = 1.7 mmol/liter, 150 mg/dl) CAPD patients had significantly higher levels of TC, LDL cholesterol, apo B, and LP-B than NTG-HD patients. There was little difference in the LP-Bc levels between NTG-CAPD, NTG-HD, and controls. Similarly, hypertriglyceridemic (HTG) CAPD patients had significantly higher TC, LDL cholesterol, apo B, and LP-B levels than HTG-HD patients. The LP-Bc levels were significantly increased in HTG-HD and HTG-CAPD patients compared with controls, but the slightly higher levels in the CAPD patients did not differ significantly from the HD group. CONCLUSION: CAPD and HD patients have a lipoprotein profile characteristic of renal failure. Patients on long-term CAPD have higher levels of cholesterol-rich apo B-containing lipoproteins unrelated to TG levels. Many patients on CAPD also have a substantial elevation of the plasma concentrations of TG-rich LPs. The clinical significance of increased levels of potentially atherogenic LP-B during CAPD remains to be investigated.  (+info)

Overexpression of human apolipoprotein A-II in mice induces hypertriglyceridemia due to defective very low density lipoprotein hydrolysis. (6/471)

Two lines of transgenic mice, hAIItg-delta and hAIItg-lambda, expressing human apolipoprotein (apo)A-II at 2 and 4 times the normal concentration, respectively, displayed on standard chow postprandial chylomicronemia, large quantities of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) but greatly reduced high density lipoprotein (HDL). Hypertriglyceridemia may result from increased VLDL production, decreased VLDL catabolism, or both. Post-Triton VLDL production was comparable in transgenic and control mice. Postheparin lipoprotein lipase (LPL) and hepatic lipase activities decreased at most by 30% in transgenic mice, whereas adipose tissue and muscle LPL activities were unaffected, indicating normal LPL synthesis. However, VLDL-triglyceride hydrolysis by exogenous LPL was considerably slower in transgenic compared with control mice, with the apparent Vmax of the reaction decreasing proportionately to human apoA-II expression. Human apoA-II was present in appreciable amounts in the VLDL of transgenic mice, which also carried apoC-II. The addition of purified apoA-II in postheparin plasma from control mice induced a dose-dependent decrease in LPL and hepatic lipase activities. In conclusion, overexpression of human apoA-II in transgenic mice induced the proatherogenic lipoprotein profile of low plasma HDL and postprandial hypertriglyceridemia because of decreased VLDL catabolism by LPL.  (+info)

Protective effect of apolipoprotein A I, A II, C I and C II on endothelial cells injury induced by low density lipoprotein. (7/471)

OBJECTIVE: To investigate the protective effect of apo-lipoprotein (apo) A I, A II, C I and C II, the main proteins in high density lipoprotein (HDL), on the morphology and function of human umbilical vein endothelial cells injured with low density lipoprotein (LDL) in vitro. METHODS: Cultured human endothelial cells derived from umbilical veins were exposed to LDL, HDL, and apoA I, A II, C I and C II. The morphology of endothelial cells was examined with phase contrast and transmission electron microscope. The released amount of lactate dehydrogenase (LDH) and 6-keto-prostaglandin F1 alpha (PGF1 alpha) was also measured. RESULTS: Endothelial cells after being injured by LDL showed cell contraction, increased release of LDH and decreased secrection of prostacyclin (PGI2). However, the addition of HDL, and apoA I, A II, C I and C II before incubation with LDL inhibited the cellular injury induced by LDL as demonstrated by lowered LDH release, increased level of PGF1 alpha and prevention of morphological changes. CONCLUSION: The results indicate that apoA I, A II, C I and C II, as well as HDL, may play an important role in combating atherogenesis by protecting endothelial cells from damages induced by LDL.  (+info)

ApoA-II maintains HDL levels in part by inhibition of hepatic lipase. Studies In apoA-II and hepatic lipase double knockout mice. (8/471)

High density lipoprotein (HDL) cholesterol levels are inversely related to the risk of developing coronary heart disease. Apolipoprotein (apo) A-II is the second most abundant HDL apolipoprotein and apoA-II knockout mice show a 70% reduction in HDL cholesterol levels. There is also evidence, using human apoA-II transgenic mice, that apoA-II can prevent hepatic lipase-mediated HDL triglyceride hydrolysis and reduction in HDL size. These observations suggest the hypothesis that apoA-II maintains HDL levels, at least in part, by inhibiting hepatic lipase. To evaluate this, apoA-II knockout mice were crossbred with hepatic lipase knockout mice. Compared to apoA-II-deficient mice, in double knockout mice there were increased HDL cholesterol levels (57% in males and 60% in females), increased HDL size, and decreased HDL cholesteryl ester fractional catabolic rate. In vitro incubation studies of plasma from apoA-II knockout mice, which contains largely apoA-I HDL particles, showed active lipolysis of HDL triglyceride, whereas similar studies of plasma from apoA-I knockout mice, which contains largely apoA-II particles, did not. In summary, these results strongly suggest that apoA-II is a physiological inhibitor of hepatic lipase and that this is at least part of the mechanism whereby apoA-II maintains HDL cholesterol levels.  (+info)

*APOA2

Apolipoprotein A-II is a protein that in humans is encoded by the APOA2 gene. This gene encodes apolipoprotein (apo-) A-II, ... Brewer HB, Lux SE, Ronan R, John KM (May 1972). "Amino acid sequence of human apoLp-Gln-II (apoA-II), an apolipoprotein ... Lackner KJ, Law SW, Brewer HB (Sep 1984). "Human apolipoprotein A-II: complete nucleic acid sequence of preproapo A-II". FEBS ... "Entrez Gene: APOA2 apolipoprotein A-II". Pussinen PJ, Jauhiainen M, Metso J, Pyle LE, Marcel YL, Fidge NH, Ehnholm C (Jan 1998 ...

*Lipoprotein lipase

Kim SY, Park SM, Lee ST (January 2006). "Apolipoprotein C-II is a novel substrate for matrix metalloproteinases". Biochem. ... Two molecules of ApoC-II can attach to each LPL dimer. It is estimated that up to forty LPL dimers may act simultaneously on a ... In the Golgi apparatus, the oligosaccharides are further altered to result in either two complex chains, or two complex and one ... "Activation of lipoprotein lipase by native and synthetic fragments of human plasma apolipoprotein C-II". Proc. Natl. Acad. Sci ...

*Hyperlipidemia

"Familial type I hyperlipoproteinemia caused by apolipoprotein C-II deficiency". Atherosclerosis. 34 (1): 53-65. doi:10.1016/ ... Hyperlipoproteinemia type II, by far the most common form, is further classified into types IIa and IIb, depending mainly on ... The lipoprotein density and type of apolipoproteins it contains determines the fate of the particle and its influence on ... For treatment of type II, dietary modification is the initial approach, but many patients require treatment with statins (HMG- ...

*APOL2

Apolipoprotein L2 is a protein that in humans is encoded by the APOL2 gene. This gene is a member of the apolipoprotein L gene ... Two transcript variants encoding the same protein have been found for this gene. GRCh38: Ensembl release 89: ENSG00000128335 - ... "Entrez Gene: APOL2 apolipoprotein L, 2". Human APOL2 genome location and APOL2 gene details page in the UCSC Genome Browser. ... McGhee KA, Morris DW, Schwaiger S (2005). "Investigation of the apolipoprotein-L (APOL) gene family and schizophrenia using a ...

*Apolipoprotein C2

1989). "A deletion mutation in the ApoC-II gene (ApoC-II Nijmegen) of a patient with a deficiency of apolipoprotein C-II". J. ... Apolipoprotein C2 or apolipoprotein C-II is a protein that in humans is encoded by the APOC2 gene. The protein encoded by this ... 1988). "Donor splice site mutation in the apolipoprotein (Apo) C-II gene (Apo C-IIHamburg) of a patient with Apo C-II ... 1989). "A nonsense mutation in the apolipoprotein C-IIPadova gene in a patient with apolipoprotein C-II deficiency". J. Clin. ...

*Low-density lipoprotein receptor-related protein 8

Apolipoprotein E (ApoE) plays an important role in phospholipid and cholesterol homeostasis. After binding ApoER2, ApoE is ... Upon reelin binding, Dab1 is phosphorylated by two tyrosine kinases, Fyn and Src. The phosphorylated Dab1 then causes further ... Riddell DR, Sun XM, Stannard AK, Soutar AK, Owen JS (2001). "Localization of apolipoprotein E receptor 2 to caveolae in the ... Herz J (June 2009). "Apolipoprotein E receptors in the nervous system". Curr. Opin. Lipidol. 20 (3): 190-6. doi:10.1097/MOL. ...

*Apolipoprotein A2

Apolipoprotein A-II is an apolipoprotein found in high density lipoprotein (HDL) cholesterol in plasma. It has an approximate ... High HDL Cholesterol (Hyperalphalipoproteinemia) at eMedicine Apolipoprotein A-II at the US National Library of Medicine ...

*Apolipoprotein C1

1988). "Two copies of the human apolipoprotein C-I gene are linked closely to the apolipoprotein E gene". J. Biol. Chem. 263 ( ... 1986). "There are two gene sequences for human apolipoprotein CI (apo CI) on chromosome 19, one of which is 4 kb from the gene ... Curry MD, McConathy WJ, Fesmire JD, Alaupovic P (1981). "Quantitative determination of apolipoproteins C-I and C-II in human ... Servillo L, Brewer HB, Osborne JC (1981). "Evaluation of the mixed interaction between apolipoproteins A-II and C-I equilibrium ...

*Acanthocyte

In liver dysfunction, apolipoprotein A-II deficient lipoprotein accumulates in plasma causing increased cholesterol in RBCs. ... Acanthocytes arise from either of two mechanisms. Alterations in membrane lipids are seen in abetalipoproteinemia and liver ... This particular cause of acanthocytosis (also known as abetalipoproteinemia, apolipoprotein B deficiency, and Bassen-Kornzweig ...

*DAB1

... and apolipoprotein E receptor-2 (ApoER2; 602600), are also required. Both receptors bound Dab1 on their cytoplasmic tails and ... "Functional dissection of Reelin signaling by site-directed disruption of Disabled-1 adaptor binding to apolipoprotein E ... 19 (2): 239-49. doi:10.1016/S0896-6273(00)80936-8. PMID 9292716. Long H, Bock HH, Lei T, Chai X, Yuan J, Herz J, Frotscher M, ... 47 (2): 165-74. doi:10.1002/gcc.20519. PMID 18008369. Deguchi K, Inoue K, Avila WE, et al. (2003). "Reelin and disabled-1 ...

*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 ...

*Reelin

Two transcription initiation sites and two polyadenylation sites are identified in the gene structure. The reelin protein ... All members of this family are receptors for Apolipoprotein E (ApoE). Therefore, they are often synonymously referred to as ' ... Moreover, the two main receptors of reelin are able to form clusters that most probably play a major role in the signaling, ... The two main reelin receptors seem to have slightly different roles: VLDLR conducts the stop signal, while ApoER2 is essential ...

*APOA5

Pennacchio LA, Olivier M, Hubacek JA, Krauss RM, Rubin EM, Cohen JC (November 2002). "Two independent apolipoprotein A5 ... Pennacchio LA, Olivier M, Hubacek JA, Krauss RM, Rubin EM, Cohen JC (November 2002). "Two independent apolipoprotein A5 ... Apolipoprotein A-V is a protein that in humans is encoded by the APOA5 gene on chromosome 11. It is significantly expressed in ... The creation of two mice models (APOA5 transgenic and APOA5 knock-out) confirmed the important role of this gene in plasma ...

*Very low-density lipoprotein

As it circulates in blood, it picks up apolipoprotein C-II (apoC-II) and additional apoE donated from high-density lipoprotein ... Nascent VLDL released from the liver contains apolipoprotein B100, apolipoprotein C1 (apoC1), apolipoprotein E (apoE), ... VLDL now meets back up with HDL where apoC-II is transferred back to HDL (but keeps apoE). HDL also transfers cholesteryl ... VLDL is assembled in the liver from triglycerides, cholesterol, and apolipoproteins. VLDL is converted in the bloodstream to ...

*DNAJB11

... modulates apolipoprotein B mRNA editing". J. Biol. Chem. 276 (49): 46445-52. doi:10.1074/jbc.M109215200. PMID 11584023. Meunier ... 12 (2): 117-26. doi:10.1093/dnares/12.2.117. PMID 16303743. Ewing RM, Chu P, Elisma F, et al. (2007). "Large-scale mapping of ... 2.0.CO;2. ISSN 1466-1268. PMC 312896 . PMID 11147971. "Entrez Gene: DNAJB11 DnaJ (Hsp40) homolog, subfamily B, member 11". Lau ...

*Liver

Examples of highly liver-specific proteins include apolipoprotein A II, coagulation factors F2 and F9, complement factor ... From below, the two additional lobes are located between the right and left lobes, one in front of the other. A line can be ... After two to five days, the umbilical vein and ductus venosus are completely obliterated; the former becomes the round ligament ... The liver is grossly divided into two parts when viewed from above - a right and a left lobe, and four parts when viewed from ...

*APOBEC1

Dance GS, Sowden MP, Cartegni L, Cooper E, Krainer AR, Smith HC (2002). "Two proteins essential for apolipoprotein B mRNA ... Apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 also known as C->U-editing enzyme APOBEC-1 is a protein that in ... Like all APOBEC proteins, A1 coordinates a zinc atom with two cysteine and one histidine residues that serve as a Lewis acid. ... Lau PP, Chang BH, Chan L (April 2001). "Two-hybrid cloning identifies an RNA-binding protein, GRY-RBP, as a component of apobec ...

*Margaret Oakley Dayhoff

... and apolipoproteins A-I, A-II, C-I and C-III. Based on this work, Dayhoff and her coworkers developed a set of substitution ... They had two daughters who became physicians, Ruth and Judith. Judith Dayhoff has a Mathematical Biophysics PhD from University ... Edward S. Dayhoff of Silver Spring; two daughters, Dr. Ruth E. Dayhoff Brannigan of College Park, and Dr. Judith E. Dayhoff of ... 2 (2): 97-98. doi:10.1089/dna.1983.2.97. ISSN 0198-0238. PMID 6347589. (Subscription required (help)). "Margaret Oakley Dayhoff ...

*Apolipoprotein E

... even if they have two ApoE4 alleles, thus reducing the risk from nine or ten times the odds of getting AD down to just two ... 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 ...

*Chylomicron

The HDL donates apolipoprotein C-II (APOC2) and apolipoprotein E (APOE) to the nascent chylomicron and, thus, converts it to a ... The main apolipoprotein component is apolipoprotein B-48 (apo B-48). While circulating in blood, chylomicrons exchange ... The triacylglycerol is then combined with phospholipids, cholesterol ester, and apolipoprotein B-48 to form a nascent ... 1-2%). They transport dietary lipids from the intestines to other locations in the body. Chylomicrons are one of the five major ...

*APOA4

Lohse P, Kindt MR, Rader DJ, Brewer HB (1990). "Human plasma apolipoproteins A-IV-0 and A-IV-3. Molecular basis for two rare ... Deeb SS, Nevin DN, Iwasaki L, Brunzell JD (1997). "Two novel apolipoprotein A-IV variants in individuals with familial combined ... Karathanasis SK (1985). "Apolipoprotein multigene family: tandem organization of human apolipoprotein AI, CIII, and AIV genes ... "Genetic polymorphism of human plasma apolipoprotein A-IV is due to nucleotide substitutions in the apolipoprotein A-IV gene". J ...

*VLDL receptor

Normal SRE-1 sequences, like those found in LDLR, are characterized by two repeats of the codon CAC separated by two ... This inability to bind LDL is due to VLDLR's incapability to bind apolipoprotein B (apoB), which is present in LDL. Receptor- ... VLDLR-II, on the other hand, lacks exon 16, which encodes for the O-glycosylation domain between sugar regions. VLDLR-III lacks ... The presence of two reelin receptors, VLDLR and ApoER2, has made it difficult to distinguish each protein's specific function. ...

*Vitellogenin lipid transport domain

Apolipoprotein B can exist in two forms: B-100 and B-48. Apoliporotein B-100 is present on several lipoproteins, including very ... Olofsson SO, Boren J (2005). "Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins ... 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

Apolipoprotein B can exist in two forms: B-100 and B-48. Apolipoprotein B-100 is present on several lipoproteins, including ... Olofsson SO, Borèn J (November 2005). "Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic ... II. Roles of juvenile hormones in adult insects". Advances in Insect Physiology. 26: 1-155. doi:10.1016/S0065-2806(08)60030-2. ... Apolipoprotein B-100 has been linked to the development of atherosclerosis. Honey bees deposit vitellogenin molecules in fat ...

*Ovarian cancer

... whereas people with two normal genes would need to acquire two mutations. In the United States, five of 100 women with a first- ... apolipoprotein A1, and transthyretin. OVA1 above 5.0 in premenopausal people and 4.4 in postmenopausal people indicates a high ... Stage II though IV tumors make up the remaining quarter of cases and have a worse prognosis, with 73-88% of patients surviving ... Two methods can be used to determine the ultrasound score and menopausal score, with the resultant scores being referred to as ...

*MODY 1

Many people with this condition have low levels of triglycerides, lipoprotein(a), apolipoproteins AII and CIII. Mutations in ... the alternative promoter of HNF4A are linked to development of type 2 diabetes.[citation needed] Stokes, A; and Duda K. ...
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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
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:
We hypothesized that impaired protection of HDL against apoB-containing lipoprotein oxidation in the 11.1 transgenic mouse model could play a role in its enhanced atherosclerosis susceptibility. This line of human apoA-II in transgenic mice presented a relative increase in the area stained with antibodies that recognize LDL oxidation epitopes compared with control or 25.3 mice. However, a concomitant increase in plasma markers of oxidative stress was not found, which suggests that the level of oxidation of plasma lipoproteins was similar in the three mouse lines studied. Thus, the main difference in oxidation susceptibility may occur in the subendothelial space. In this milieu, the antioxidant and anti-inflammatory properties of HDL may confer vital protection.38. Lipoproteins that undergo oxidation are known to increase their electrophoretic mobility. This property can be used to establish the degree of LDL oxidation and has been used previously to assess HDL protectivity.39 Using this ...
All reagents should be stored refrigerated (2-8°C). Return all reagents to 2-8°C promptly after use. Unopened reagents can be used for one year from the date of manufacture, as indicated by the expiration date on the package and bottle labels. Opened reagents can be used for one month if stored at 2-8°C ...
Women have significantly higher plasma concentrations of high-density lipoprotein (HDL) and apolipoprotein (apo) A-I than men. Human HDL consists of two major species of apoA-I-containing lipoproteins: LpA-I (lipoprotein containing apoA-I but not apoA-II) and LpA-I:A-II (lipoprotein containing both apoA-I and apoA-II). LpA-I is itself heterogeneous and contains several subclasses of different size and composition. We analyzed LpA-I subclasses in 12 male and 12 female healthy normolipidemic adults. LpA-I concentrations were significantly higher in women (72.4 +/- 5.6 mg/dL) than in men (50.2 +/- 2.2 mg/dL) (P , .05). LpA-I was preparatively isolated from fasting plasma by immunoaffinity chromatography. Gel filtration chromatography was then used to isolate LpA-I subclasses based on size. Three major subclasses were eluted: large, medium, and small LpA-I. No differences between men and women in the size or composition of individual LpA-I subclasses were observed. In contrast, the distribution and ...
Mouse Apolipoprotein E SimpleStep ELISA® Kit is a highly sensitive (130 pg/ml), single-wash 90 min immunoassay suitable for Serum, Heparin Plasma, EDTA Plasma, Citrate Plasma samples.
The systemic amyloidoses are a number of disorders of varying etiology characterized by extracellular protein deposition. The most common form is an acquired amyloidosis secondary to multiple myeloma or monoclonal gammopathy of unknown significance (MGUS) in which the amyloid is composed of immunoglobulin light chains. In addition to light chain amyloidosis, there are a number of acquired amyloidoses caused by the misfolding and precipitation of a wide variety of proteins. There are also hereditary forms of amyloidosis.. The hereditary amyloidoses comprise a group of autosomal dominant, late-onset diseases that show variable penetrance. A number of genes have been associated with hereditary forms of amyloidosis, including those that encode transthyretin, apolipoprotein AI, apolipoprotein AII, fibrinogen alpha chain, gelsolin, cystatin C and lysozyme. Apolipoprotein AI, apolipoprotein AII, lysozyme, and fibrinogen amyloidosis present as non-neuropathic systemic amyloidosis, with renal dysfunction ...
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Objectives- Subjects with the metabolic syndrome (MetS) have reduced HDL concentration and altered metabolism of HDL Lipoprotein (Lp) A-I and LpA-I:A-II particles. In MetS, fenofibrate and atorvastatin may have differential effects on HDL particle kinetics.. Research Design and Methods- Eleven men with MetS were studied in a randomized double-blinded crossover trial of 5-week intervention periods with placebo, fenofibrate (200mg/day) and atorvastatin (40mg/day). LpA-I and LpA-I:A-II kinetics were examined using stable isotopic techniques and compartmental modelling.. Results- Compared with placebo, fenofibrate significantly increased the production of both LpA-I:A-II (+30%, P,0.001) and apoA-II (+43%, P , 0.001), accounting for significant increases of their corresponding plasma concentrations (+10% and +23% respectively), but it did not alter LpA-I kinetics or concentration. Atorvastatin did not significantly alter HDL-cholesterol concentration or the kinetics of HDL particles.. Conclusions- In ...
Apolipoprotein A2 antibody (HRP) (apolipoprotein A-II) for ELISA. Anti-Apolipoprotein A2 pAb (GTX40825) is tested in Human samples. 100% Ab-Assurance.
Reverse cholesterol transport (RCT), the transfer of cholesterol from peripheral tissues, including the subendothelial space of the arterial wall, to the liver for disposal, is a current model of HDL atheroprotection. The final RCT step, selective hepatic HDL-cholesteryl ester (CE) uptake, is mediated by scavenger receptor class B type I (SR-BI). The net receptor reaction of SR-BI vs. HDL is distinct from that of LDL vs. the LDL receptor. LDL holo particle uptake is succeeded by steps that breakdown apo B-100 and hydrolyze and recycle the CE. In contrast, HDL-CE uptake is selective, occurring without a concomitant net uptake of the major HDL protein, apo A-I and even though apo E and apo A-I bind equally well to SR-BI, apoA-I-containing particles mediate 2-fold more selective CE uptake. The reaction of HDL with SR-BI is similar to the activity of a streptococcal serum opacity factor (SOF) against HDL_both reactions selectively remove CE from HDL leaving remnants. In addition, SOF catalyzes the ...
Objective: Classical phenylketonuria (PKU) is an inborn error of metabolism characterized by high Phenylalanine (Phe) levels in blood and treated with a special low Phe diet which can be defined as "nonatherogenic". Since coronary heart disease (CHD) was reported to be a disease of zinc and copper imbalance, we aimed indirectly to evaluate the effect of the special diet on the size of LDL particles and to investigate whether some minerals and trace elements are involved in their lipoprotein metabolism. Methods: Eighty-six (N=86) PKU patients were divided into two groups. Group A (N=44) on a strict diet and group B (N=42) who did not adhere to their treatment. Healthy children (N=98) were the controls. Serum total cholesterol (t-Chol), triacylglycerol, High-density lipoprotein (HDL) and t-Chol in very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) were measured with enzymatic methods, whereas Apolipoprotein AI (Apo AI), Apolipoprotein AII (Apo AII) and Apolipoprotein B (Apo B) ...
Changes in circulating lipoproteins, which may be related to the risk for atherosclerotic vascular disease, were studied in a control group and in two groups of 24 or 26 women using different preparations of low-dose oral contraceptives for 3 months. One preparation contained 150 μg levo-norgestrel and 30 μg ethinylestradiol (Stediril-d 150/30); the other contained 750 μg lynestrenol and 37.5 μg ethinylestradiol (Ministat). No significant changes were found with either of the preparations in serum cholesterol or high density lipoprotein cholesterol (HDL-C) levels. Apolipoprotein A-II levels increased during Ministat treatment from 50.4 to 61.4 mg/dL and during Stediril-d 150/30 treatment from 52.7 to 58.9 mg/dL (both P , 0.001). These changes differed significantly from each other (P , 0.01). Apolipoprotein A-I levels increased significantly during use of Ministat only. Apoliprotein B in low density lipoprotein increased by about 20% (P , 0.001) in both groups. Post-heparin lipoprotein ...
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 F (apoF) is a 35 kDa protein encoded by a cDNA cloned from the murine lacrimal gland. In the present paper, the murine apoF has been expressed as a recombinant histidine-tagged protein in Escherichia coli and purified from expressing cultures. We report here the unique distinctions of apoF including comparisons of apoF with other apolipoproteins (apoD, apoE, and apoN), as well as why this protein was produced. The data presented here provide evidence that isolated recombinant apoF purified in the experimental conditions described here can be used for functional studies ...
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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 ...
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High - resolution two - dimension electrophoresis technique for protein with silver staining was used to characterise urinary high density lipoprotein (HDL) - apolipoproteins. Sequential ultracentrufugation method was used to isolate urinary lipoprotein particles of the same density as serum HDL. Immunostaining of electroblotted proteins further confirmed the presence of HDL-Apos in urine. HDL - Apolipoprotein A-I, A-II and C were identified in urine of normal subjects, diabetic patients and patients with biopsy proven glomerular proteinuria. An in-house ELISA method was used to quantify urinary HDL - Apo A - I. Selectivity indices were also determined.
Abstract: Enzyme-linked immunosorbent assay (ELISA) has been used formeasuring apolipoproteins A-I and B in the urine. ApoB is absentin urine of healthy subjects, and apoA-I is determined in tracequantity. In patients with chronic glomerulonephritis quantity ofapoA-I in urine was 117 times as much as in control group. ApoBis present in urine of patients in considerable quantity(1528*315 *g/l).) The ELISA method for determining apoA-I andapoB in urine makes it possible to evaluate the gravity ofpathological process in kidney ...
Plasma triglyceride levels have been correlated with insulin levels in both normal populations and in patients with endogenous hypertriglyceridemia (1). As a result of this reproducible significant association, it has been suggested that hyperinsulinism might be causally related to endogenous hypertriglyceridemia (2).. It has now been established that "endogenous hypertriglyceridemia" describes a heterogenous group of primary familial and sporadic disorders. Recently two common forms of monogenic hypertriglyceridemia have been described: "pure" monogenic familial hypertriglyceridemia, in which the hypertriglyceridemic propositus comes from a family in which all affected relatives have isolated hypertriglyceridemia; and familial combined hyperlipidemia, in which the hypertriglyceridemic propositus ...
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Lipoprotein, illustration. This is a high density lipoprotein (HDL), or good cholesterol, molecule. It consists of a core of esterified cholesterol molecules surrounded by a shell of unesterified cholesterol (orange with violet cap) and phospholipids (orange with blue cap). The complex structure includes carrier proteins (green) known as apolipoproteins, which assist transport in the blood. HDL cholesterol plays a role in fat metabolism and contributes to cardiovascular health. - Stock Image F012/8897
Apolipoproteins function as structural components of lipoprotein particles, cofactors for enzymes, and ligands for cell-surface receptors. Most of the apoliporoteins exhibit proteoforms, arising from single nucleotide polymorphisms (SNPs) and post-translational modifications such as glycosylation, oxidation, and sequence truncations. Reviewed here are recent studies correlating apolipoproteins proteoforms with the specific clinical measures of lipid metabolism and cardiometabolic risk. Targeted mass spectrometric immunoassays toward apolipoproteins A-I, A-II, and C-III were applied on large cross-sectional and longitudinal clinical cohorts. Several correlations were observed, including greater apolipoprotein A-I and A-II oxidation in patients with diabetes and cardiovascular disease, and a divergent apoC-III proteoforms association with plasma triglycerides, indicating significant differences in the metabolism of the individual apoC-III proteoforms. These are the first studies of their kind, correlating
Apolipoproteins have multiple roles. One role is to increase the overall solubility of the lipid particle, helping it to dissolve in the aqueous environment of the blood (apolipoproteins are amphipathic, or detergent-like proteins). Apolipoproteins can also function as enzyme co-factors (receptor ligands), facilitating the transfer of their lipid cargo to specific cells. Thus, the apoliproteins are the "smart" or working-end of the lipoprotein particle. The apolipoproteins dictate where the particles will dock and where they can bind, and in so doing the apolipoproteins regulate lipid metabolism in the body. So although the particles are composed of phospholipids and have lipid cargo, the few proteins on their surface are what give them their collective name of lipoproteins ...
Silver-staining of immunoprecipitates extends the sensitivity of the radial immunodiffusion assay by tenfold. This modification permits the quantification of apolipoproteins A-I, A-II, C, and E at levels of 0.2-1.0 mg/dl in plasma samples at a sensitivity threshold of 10 ng. The silver-enhanced radial immunodiffusion method is readily adapted from the standard method, simple and inexpensive to perform, and does not require costly instrumentation. These advantages make the modified RID assay an attractive alternative to other forms of immunoassay.
Apolipoproteins have important structural and functional roles in several lipoprotein particles. Apolipoproteins regulate lipid metabolism, adipose tissue, and energy production and serve major...
ABCA1 expression and co-localization with [1-93]ApoA-I and ApoA-I. (A) Western blot analysis with anti-ABCA1 antibodies of cell lysates prepared from HepG2 ce
There is no way to know for certain, by some experts estimate that the feral cat population in North America may equal or even exceed that of the "owned cat population. Feral cats are not socialized to humans and avoid contact with people whenever possible. In contrast, "stray" cats are often those cats that have left a home or have been abandoned by their owners. These strays may have been socialized to humans at one time and will often approach people and may even allow petting. All cats, feral, stray and owned cats that simply roam the neighborhood are all members of the domestic species, Felis catus.. Traditionally, feral and stray cats are trapped whenever possible and then are taken to local animal shelters. Once at a shelter, if they are socialized to humans and have a calm disposition, some cats may be adopted out. However, the vast majority of these feral cats may be harboring diseases, such as Feline Leukemia, or they are totally wild and cannot be adopted out. These cats will often ...
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Understanding the determinants of HDL function is widely considered a critical priority in HDL research. Given the heterogeneity of HDL species in the circulation, understanding the transporters essential for cholesterol efflux and the HDL species, which are the major contributors to this process may direct contemporary strategies to optimize HDL function or deliver novel HDL analogues in vivo. The present study, which represents the most detailed evaluation of HDL particle size and cellular cholesterol efflux via ABCA1 and ABCG1 to date, has identified HDL size as a key determinant of the efflux capacity of HDL. We further demonstrate that ABCA1 is a quantitatively critical mediator of cholesterol efflux to HDL3, and that HDL3b, HDL3c and lipid-free apoA-I are all suitable therapeutic targets for optimizing cellular cholesterol efflux.. It is a widely held view that ABCA1 is an important mediator of cholesterol export and that it specifically requires apolipoproteins (such as apoA-I) that ...
Site-directed mutagenesis and other molecular biology-based techniques are now available for probing the amphipathic alpha-helix structural motif in the exchangeable apolipoproteins. Here we survey the published literature on lipid-binding and functional domains in apolipoproteins A-I, A-II, A-IV, C-I, C-II, C-III, and E and compare these results with recently developed computer methods for analysis of the location and properties of amphipathic helixes. This comparison suggests that there are at least three distinct classes of amphipathic helixes (classes A, Y, and G*) in the exchangeable apolipoproteins whose distribution varies within and between the seven apolipoproteins. This comparison further suggests that lipid affinity resides largely in class A amphipathic helixes (Segrest, J. P., et al. 1990. Proteins. 8: 103) and that variations in structure and/or numbers of class A domains in individual apolipoproteins allow a range of lipid affinities from high to low. The positions of the four a ...
Apolipoprotein A-I (apo A-I) is the most abundant protein in high-density lipoprotein (HDL) particles, and it plays an important role in HDL metabolism. Both apo A-I and HDL cholesterol (HDL-C) levels are inversely associated with risk of cardiovascular disease. Segregation analyses suggest apo A-I levels are under the control of one or more major loci. Since HDL particles are heterogeneous in their composition and size, genetic influence on its subfractions (i.e., HDL2 and HDL3) could vary. A previous report showed evidence of a major locus controlling HDL3-C levels in a subset of the current study population. Because quantitative trait loci involved in complex diseases are likely to have pleiotropic effects on several related traits, it is possible to have a common major gene involved in regulating apo A-I and HDL3-C levels. We performed a bivariate segregation analysis of apo A-I and HDL3-C levels in 1,006 individuals from 137 families ascertained through probands undergoing elective, diagnostic
A lipid metabolism disorder characterized by elevated triglyceride levels as a result of excess hepatic production of VLDL or heterozygous LPL deficiency.
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 ...
UCL Discovery is UCLs open access repository, showcasing and providing access to UCL research outputs from all UCL disciplines.
ProSpecs Apolipoproteins include: Clusterin Human Recombinant, Clusterin Rat Recombinant, Apolipoprotein-D Human Recombinant, Human Apolipoprotein-J, Apolipoprotein-J Canine Recombinant
0.5mg/ml if reconstituted with 0.2ml sterile DI water. Eukaryotic initiation factor 4A-II is a protein that in humans is encoded by the EIF4A2 gene. …
For US: For Research Use Only. This kit is optimized for being used with the HEMOCLOT LA-S and HEMOCLOT LA-C assays. See product page for more information.
Article: We report studies of the interaction of Alzheimers amyloid beta protein (Aβ) with normal human plasma high density lipoprotein (HDL), aiming to clarify to which lipoprotein (LP) structural constituent (apolipoprotein or lipid) soluble Aβ is primarily bound. Purified HDLs were incubated wit...
Considerable attention has focused on the development of new therapeutic agents that substantially elevate levels of HDL-C. However, development of pharmacological therapies that raise HDL-C levels has been challenging, in part because the underlying biology is substantially more complex than other lipoprotein-directed therapies. HDL circulates in many forms, including both lipid-rich and lipid-poor subfractions (12). It appears that lipid-poor preβ1-HDL fractions acquire cholesterol from macrophages in atherosclerotic plaques. These particles increase in size as they accumulate cholesterol. Cholesterol is ultimately taken up by the liver from these larger, lipid-rich α1-HDL particles or transferred to apoB-containing particles, a process known as RCT (13). Preβ1-HDL represents the most efficient substrate for enhancing RCT, which is considered a pivotal mechanism underlying the potential benefits of HDL-C-raising therapies (14). Because apoA-I has the capacity to generate more lipid-poor ...
References for Abcams Human Apolipoprotein A I peptide (ab66674). Please let us know if you have used this product in your publication
Apolipoproteins AI/B/E gene polymorphism and their plasma levels in patients with coronary artery disease in a tertiary care-center of Eastern India ...
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。
Apolipoprotein A1 antibody [5F4F5] (apolipoprotein A-I) for ELISA, WB. Anti-Apolipoprotein A1 mAb (GTX83043) is tested in Human samples. 100% Ab-Assurance.
High-density lipoprotein is predominantly composed of the apolipoproteins apoAI and apoAII. These apolipoproteins are responsible for collecting lipids from arteries and transporting them back to the liver for reutilization, which provides protection against cardiovascular diseases. While many studies examine the cardiovascular effects of HDL and its apolipoproteins, few have looked at whether these molecules maintain the health of other bodily systems and organs. In this study, the authors show that apoA1 maintains pulmonary function in mice. Along with inhibiting stressors such as proinflammatory HDL formation and the activity of paranoxonase 1 (PON1) and 3-nitrotyrosine (3NT) in the plasma, apoA1 was shown to limit pulmonary inflammation and oxidative stress markers, such as 3NT, 4-hydroxynonenal adducts (4-HNE), transforming growth factor-β (TGFβ), xanthineoxidase, myeloperoxidase and endothelial nitric oxide synthase in the lung milieu. Additionally, apoA1 was shown to enhance arterial ...
Recombinant Human Apolipoprotein A I Full length protein datasheet (ab50239). Abcam offers quality products including antibodies, assays and other reagents.
Investigation of variants identified in caucasian genome-wide association studies for plasma high-density lipoprotein cholesterol and triglycerides levels in Mexican dyslipidemic study samples. ...
Recombinant mammalian apolipoproteins have been expressed in a variety of cultured mammalian cell lines (Reardon et al. 1986; Mallory et al. 1987; Blackhart et al. 1990; Yao et al. 1991), transgenic...
Apolipoprotein L 5山羊多克隆抗体(ab79281)可与人样本反应并经WB, ELISA实验严格验证。所有产品均提供质保服务,中国75%以上现货。
Windows 8 currently still in its pre-beta phase of development, has an official build number for 8176. Microsoft is slated to release the Beta of its next version of operating system sometime in late February. Today, a

The circularization of amyloid fibrils formed by apolipoprotein C-II. - Semantic ScholarThe circularization of amyloid fibrils formed by apolipoprotein C-II. - Semantic Scholar

One striking example is the remarkable ability of human apolipoprotein C-II amyloid fibrils to circularize and form closed ... Our results suggest a model for apoC-II fibrils as ribbons approximately 2.1-nm thick and 13-nm wide with a helical repeat ... We use these observed biophysical properties to model the apoC-II amyloid fibrils either as wormlike chains or using a random- ... More generally, the ability of apoC-II fibrils to form rings also highlights the degree to which the common cross-beta ...
more infohttps://www.semanticscholar.org/paper/The-circularization-of-amyloid-fibrils-formed-by-a-Hatters-MacRaild/46f282cb627acdd83087a34adf42cd5ca7aa4638

A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations  ...A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations ...

Lipid-free human apolipoprotein C-II (apoC-II) forms characteristic amyloid fibrils and is one of several apolipoproteins that ... A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations ... A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations. ... Our structural model for apoC-II fibrils suggests that apoC-II monomers fold and self-assemble to form a stable cross-beta- ...
more infohttps://edoc.unibas.ch/21186/

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 ...
more infohttps://dnalabsindia.com/ngs-test-apolipoprotein-c-ii-deficiency-apoc2-cost-c49.html

Familial amyloidosis - definition of familial amyloidosis by The Free DictionaryFamilial amyloidosis - definition of familial amyloidosis by The Free Dictionary

familial apolipoprotein C-II (apo C-II) deficiency. *familial apolipoprotein C-II (apo C-II) deficiency ... familial apolipoprotein C-II (apo C-II) deficiency. *familial apolipoprotein C-II (apo C-II) deficiency ...
more infohttp://www.thefreedictionary.com/familial+amyloidosis

Correlations between Apolipoprotein D (APOD) and DESCorrelations between Apolipoprotein D (APOD) and DES

DES regulates expression of avian apolipoprotein D during regression and recrudescence of the oviduct and epithelial-derived ... Correlations between Apolipoprotein D (APOD) and DES. Diethylstilbestrol regulates expression of avian apolipoprotein D during ... Apolipoprotein D featured image credit opm.phar.umich.edu.. DES DIETHYLSTILBESTROL RESOURCES. *Source DES and epigenetics ... Apolipoprotein D (APOD) is a glycoprotein which is widely expressed in mammalian tissues. It is structurally and functionally ...
more infohttps://diethylstilbestrol.co.uk/apod/

Association of Backfat Thickness with Postheparin Lipoprotein Lipase Activity and Very Low Density Lipoprotein-Subfractions in...Association of Backfat Thickness with Postheparin Lipoprotein Lipase Activity and Very Low Density Lipoprotein-Subfractions in...

It is believed that the apolipoprotein E, which is present in higher quantities in VLDL-subfraction 2 plays an important role ... No differences were observed in postheparin plasma LPL activity and backfat thickness for two lines of pigs. There were ... TEL : +82-2-888-6558 FAX : +82-2-888-6559 E-mail : [email protected] Copyright © 2020 by Asian-Australasian Journal of Animal ... Sixteen pigs from 2 distinct genetic lines (LGAH and VFIL) obtained after eight generations of divergent selection for high (H ...
more infohttps://www.ajas.info/journal/view.php?number=20027

Modulation of Apolipoprotein D levels in human pregnancy and association with gestational weight gain | Reproductive Biology...Modulation of Apolipoprotein D levels in human pregnancy and association with gestational weight gain | Reproductive Biology...

We investigated the changes in the levels of ApoD in the plasma of pregnant women at the two first trimesters of gestation and ... Apolipoprotein D (ApoD) is a lipocalin involved in several processes including lipid transport, but its modulation during human ... From: Modulation of Apolipoprotein D levels in human pregnancy and association with gestational weight gain ... ApoD levels were measured in women with a BMI of 20-26 kg/m2 and a GWG of 11-18 kg at the two first trimesters of pregnancy ( ...
more infohttps://rbej.biomedcentral.com/articles/10.1186/1477-7827-7-92/figures/1

Literature: Apolipoprotein A-II (ApoA-II) (IPR006801) | InterPro | EMBL-EBILiterature: Apolipoprotein A-II (ApoA-II) (IPR006801) | InterPro | EMBL-EBI

Literature: Apolipoprotein A-II (ApoA-II) (IPR006801). References used in this entry. The following publications were referred ... Structures of apolipoprotein A-II and a lipid-surrogate complex provide insights into apolipoprotein-lipid interactions.. Kumar ... Apolipoprotein A-II, HDL metabolism and atherosclerosis.. Tailleux A, Duriez P, Fruchart JC, Clavey V.. Atherosclerosis 164 1- ... Purification, primary structure, and antimicrobial activities of bovine apolipoprotein A-II.. Motizuki M, Itoh T, Yamada M, ...
more infohttp://www.ebi.ac.uk/interpro/entry/IPR006801/literature

Anti-Apolipoprotein A II antibody (ab27627) | AbcamAnti-Apolipoprotein A II antibody (ab27627) | Abcam

Sheep polyclonal Apolipoprotein A II antibody validated for WB, ELISA and tested in Human. Immunogen corresponding to full ... Anti-Apolipoprotein A II antibody. See all Apolipoprotein A II primary antibodies. ... Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. ...
more infohttp://www.abcam.com/Apolipoprotein-A-II-antibody-ab27627.html

Anti-Apolipoprotein A II antibody (ab85749) | AbcamAnti-Apolipoprotein A II antibody (ab85749) | Abcam

Goat polyclonal Apolipoprotein A II antibody validated for WB, IP, ELISA, IHC and tested in Human. Immunogen corresponding to ... Anti-Apolipoprotein A II antibody. See all Apolipoprotein A II primary antibodies. ... This antibody recognises Human Apolipoprotein A II. Exhibits very low cross reactivity with Type A I, B, C I, C II, C III, E ... Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Apolipoprotein A II antibody (ab85749) ...
more infohttp://www.abcam.com/apolipoprotein-a-ii-antibody-ab85749.html

Apolipoprotein A-II/ApoA2 Antibodies: Novus BiologicalsApolipoprotein A-II/ApoA2 Antibodies: Novus Biologicals

Browse our Apolipoprotein A-II/ApoA2 Antibody catalog backed by our Guarantee+. ... Apolipoprotein A-II/ApoA2 Antibodies available through Novus Biologicals. ... anti-apolipoprotein A-II antibody, anti-Apolipoprotein A2 antibody. 3 Results for "apolipoprotein-a-ii-apoa2" in Primary ... Alternate Names for Apolipoprotein A-II/ApoA2 Antibodies. anti-Apolipoprotein A-II/ApoA2 antibody, anti-APOA2 antibody, anti- ...
more infohttps://www.novusbio.com/primary-antibodies/apolipoprotein-a-ii-apoa2?preservative=No%20Preservative&related_diseases=Dyslipidemias

Apolipoprotein A-II/ApoA2 Antibodies: Novus BiologicalsApolipoprotein A-II/ApoA2 Antibodies: Novus Biologicals

Browse our Apolipoprotein A-II/ApoA2 Antibody catalog backed by our Guarantee+. ... Apolipoprotein A-II/ApoA2 Antibodies available through Novus Biologicals. ... anti-apolipoprotein A-II antibody, anti-Apolipoprotein A2 antibody. 6 Results for "apolipoprotein-a-ii-apoa2" in Primary ... Alternate Names for Apolipoprotein A-II/ApoA2 Antibodies. anti-Apolipoprotein A-II/ApoA2 antibody, anti-APOA2 antibody, anti- ...
more infohttps://www.novusbio.com/primary-antibodies/apolipoprotein-a-ii-apoa2?related_diseases=Malignant%20Neoplasms

RCSB PDB 









- 1BY6: Peptide of human apolipoprotein C-II Literature Report PageRCSB PDB - 1BY6: Peptide of human apolipoprotein C-II Literature Report Page

Structure of a biologically active fragment of human serum apolipoprotein C-II in the presence of sodium dodecyl sulfate and ... APOLIPOPROTEIN C-II A 36 Homo sapiens Fragment: RESIDUES 44-79 Gene Name(s): APOC2 Gene View APC2 Gene View ... RCSB PDB (citation) is managed by two members of the Research Collaboratory for Structural Bioinformatics: Rutgers and UCSD/ ...
more infohttp://www.rcsb.org/pdb/explore/litView.do?structureId=1BY6

Product Overview anti-Apolipoprotein C-II AntibodiesProduct Overview anti-Apolipoprotein C-II Antibodies

Selected quality suppliers for anti-Apolipoprotein C-II antibodies. ... Order monoclonal and polyclonal Apolipoprotein C-II antibodies for many applications. ... More Antibodies against Apolipoprotein C-II Interaction Partners. Zebrafish Apolipoprotein C-II (APOC2) interaction partners ... Additionally we are shipping Apolipoprotein C-II Kits (51) and Apolipoprotein C-II Proteins (28) and many more products for ...
more infohttp://www.antibodies-online.com/abstract/Apolipoprotein+C-II+

Sequence Similarity 









- 1BY6: Peptide of human apolipoprotein C-II Sequence Similarity Report PageSequence Similarity - 1BY6: Peptide of human apolipoprotein C-II Sequence Similarity Report Page

Structure of a biologically active fragment of human serum apolipoprotein C-II in the presence of sodium dodecyl sulfate and ... RCSB PDB (citation) is managed by two members of the Research Collaboratory for Structural Bioinformatics: Rutgers and UCSD/ ... ACTION - (A) Select for download / view details OR (B) Select two chains for comparison ... You can also use the structure comparison tool to compare any 2 given structures. ...
more infohttp://www.rcsb.org/pdb/explore/sequenceCluster.do?structureId=1BY6&entity=1&seqid=95

apoa2, apolipoprotein A-II - Creative Biogeneapoa2, apolipoprotein A-II - Creative Biogene

APOA2; apolipoprotein A-II; apoAII; Apo-AII; ApoA-II; apolipoprotein A2; cb1032; wu:fb57h11; zgc:193613; uncharacterized ... This gene encodes apolipoprotein (apo-) A-II, which is the second most abundant protein of the high density lipoprotein ... Defects in this gene may result in apolipoprotein A-II deficiency or hypercholesterolemia. [provided by RefSeq, Jul 2008] ... The protein is found in plasma as a monomer, homodimer, or heterodimer with apolipoprotein D. ...
more infohttps://www.creative-biogene.com/symbolsearch_apoa2.html

APOA2 - apolipoprotein A-IIAPOA2 - apolipoprotein A-II

A-II is the second most abundant protein of the high density lipoprotein particles. The apo-A-II gene consists of 4 exons and 3 ... Familial apo-A-II deficiency may result from a splice-junction alteration which blocks splicing of intron 3 from the primary ... Apolipoprotein (Apo-) A-II is the second most abundant protein of the high density lipoprotein particles. The apo-A-II gene ... Familial apo-A-II deficiency may result from a splice-junction alteration which blocks splicing of intron 3 from the primary ...
more infohttp://www.urogene.org/kgdb/gene/55.html

Anti-Apolipoprotein A-II Antibody | Goat anti-Human Polyclonal AP | LSBioAnti-Apolipoprotein A-II Antibody | Goat anti-Human Polyclonal AP | LSBio

Apolipoprotein A-II antibody LS-C505484 is an AP-conjugated goat polyclonal antibody to human Apolipoprotein A-II. Validated ... Apolipoprotein A-II antibody LS-C505484 is an AP-conjugated goat polyclonal antibody to human Apolipoprotein A-II. Validated ... Apolipoprotein A-II antibody LS-C505484 is an AP-conjugated goat polyclonal antibody to human Apolipoprotein A-II. Validated ... Popular Apolipoprotein A-II Products. Apolipoprotein A‑II Antibody (clone 4F3) IHC‑plus™ LS‑B4280 ...
more infohttps://www.lsbio.com/antibodies/apolipoprotein-a-ii-antibody-ap-elisa-ls-c505484/519045

Human Apolipoprotein A-II Enrichment Displaces Paraoxonase From HDL and Impairs Its Antioxidant Properties | Circulation...Human Apolipoprotein A-II Enrichment Displaces Paraoxonase From HDL and Impairs Its Antioxidant Properties | Circulation...

Apolipoprotein A-II (apoA-II), the second major high-density lipoprotein (HDL) apolipoprotein, has been linked to familial ... HDLs are classified according to their content of major apolipoproteins: apolipoprotein A-I (apoA-I) and apoA-II. ApoA-I plays ... Expression of human apolipoprotein A-II in apolipoprotein E-deficient mice induces features of familial combined hyperlipidemia ... II. Evidence for direct reduction of lipid hydroperoxides by methionine residues of apolipoproteins AI and AII. J Biol Chem. ...
more infohttp://circres.ahajournals.org/content/95/8/789

Abstract 102: Profound Exclusion of Apolipoprotein A-II from Selective Hepatic Cholesteryl Ester Uptake | Arteriosclerosis,...Abstract 102: Profound Exclusion of Apolipoprotein A-II from Selective Hepatic Cholesteryl Ester Uptake | Arteriosclerosis,...

HDL-apo A-I and apo A-II. Cellular uptake of HDL-[3H]CE labeled with [125I]apo A-I or [125I]apo A-II was compared in CHO-K1 and ... Abstract 102: Profound Exclusion of Apolipoprotein A-II from Selective Hepatic Cholesteryl Ester Uptake. Baiba K Gillard, G. R ... Relative to CE, both apo A-I and apo A-II were excluded from uptake by all cells. However, relative to the apo A-I and apo A-II ... Abstract 102: Profound Exclusion of Apolipoprotein A-II from Selective Hepatic Cholesteryl Ester Uptake ...
more infohttp://atvb.ahajournals.org/content/33/Suppl_1/A102

Lipids Enhance Apolipoprotein C-II-Derived Amyloidogenic Peptide Oligomerization but Inhibit Fibril FormationLipids Enhance Apolipoprotein C-II-Derived Amyloidogenic Peptide Oligomerization but Inhibit Fibril Formation

314000-lipids-enhance-apolipoprotein-c-ii-derived-amyloidogenic-peptide-oligomerization-but-inhibit-fibril-formation. ... Lipids Enhance Apolipoprotein C-II-Derived Amyloidogenic Peptide Oligomerization but Inhibit Fibril Formation. ...
more infohttps://findanexpert.unimelb.edu.au/scholarlywork/314000-lipids-enhance-apolipoprotein-c-ii-derived-amyloidogenic-peptide-oligomerization-but-inhibit-fibril-formation

Modulation of Kinin B2 Receptor Signaling Controls Aortic Dilatation and Rupture in the Angiotensin II-Infused Apolipoprotein E...Modulation of Kinin B2 Receptor Signaling Controls Aortic Dilatation and Rupture in the Angiotensin II-Infused Apolipoprotein E...

angiotensin II. AoSMC. aortic smooth muscle cell. ApoE−/−. apolipoprotein E-deficient. AT1R. angiotensin II type 1 receptor. ... Approach and Results-AAA was induced in apolipoprotein E-deficient mice via infusion of angiotensin II (1.0 μg/kg per minute SC ... Modulation of Kinin B2 Receptor Signaling Controls Aortic Dilatation and Rupture in the Angiotensin II-Infused Apolipoprotein E ... Osteoprotegerin deficiency limits angiotensin II-induced aortic dilatation and rupture in the apolipoprotein E-knockout mouse. ...
more infohttp://atvb.ahajournals.org/content/36/5/898

Inhibition of Endoplasmic Reticulum Stress and Atherosclerosis by 2-Aminopurine in Apolipoprotein E-Deficient MiceInhibition of Endoplasmic Reticulum Stress and Atherosclerosis by 2-Aminopurine in Apolipoprotein E-Deficient Mice

Y. Zhao, Z. Guo, X. Lin et al., "Apolipoprotein E-deficient lipoproteins induce foam cell formation by activation of PERK-EIF-2 ... J. A. Piedrahita, S. H. Zhang, J. R. Hagaman, P. M. Oliver, and N. Maeda, "Generation of mice carrying a mutant apolipoprotein ... A. H. Hasty, M. F. Linton, L. L. Swift, and S. Fazio, "Determination of the lower threshold of apolipoprotein E resulting in ... D. Wu, C. Sharan, H. Yang et al., "Apolipoprotein E-deficient lipoproteins induce foam cell formation by downregulation of ...
more infohttps://www.hindawi.com/journals/isrn/2013/847310/ref/

Apolipoprotein A-II, Human Plasma, High-Density Lipoprotein | 178455Apolipoprotein A-II, Human Plasma, High-Density Lipoprotein | 178455

High-Density Lipoprotein Native apolipoprotein A-II from human plasma. The second most abundant protein of HDL. Binds to ... Apolipoprotein A-II, Human Plasma, High-Density Lipoprotein. 178455 Sigma-AldrichApolipoprotein A-II, Human Plasma, High- ... Apo A-II. Description. Native apolipoprotein A-II from human plasma. Shown to bind to phospholipids during lipoprotein ... Native apolipoprotein A-II from human plasma. The second most abundant protein of HDL. Binds to phospholipids during ...
more infohttp://www.emdmillipore.com/US/en/product/Apolipoprotein-A-II-Human-Plasma-High-Density-Lipoprotein,EMD_BIO-178455

Absence of CC chemokine receptor-2 reduces atherosclerosis in apolipoprotein E-deficient mice.  - PubMed - NCBIAbsence of CC chemokine receptor-2 reduces atherosclerosis in apolipoprotein E-deficient mice. - PubMed - NCBI

Absence of CC chemokine receptor-2 reduces atherosclerosis in apolipoprotein E-deficient mice.. Dawson TC1, Kuziel WA, Osahar ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/10208497?dopt=Abstract
  • X-ray diffraction analysis of aligned apoC-II fibrils indicated a simple cross-beta-structure composed of two parallel beta-sheets. (unibas.ch)
  • Examination of apoC-II fibrils using transmission electron microscopy, scanning transmission electron microscopy, and atomic force microscopy indicated that the fibrils are flat ribbons composed of one apoC-II molecule per 4.7-A rise of the cross-beta-structure. (unibas.ch)
  • Cross-linking results using single-cysteine substitution mutants are consistent with a parallel in-register structural model for apoC-II fibrils. (unibas.ch)
  • Fluorescence resonance energy transfer analysis of apoC-II fibrils labeled with specific fluorophores provided distance constraints for selected donor-acceptor pairs located within the fibrils. (unibas.ch)
  • These findings were used to develop a simple 'letter-G-like' beta-strand-loop-beta-strand model for apoC-II fibrils. (unibas.ch)
  • Our structural model for apoC-II fibrils suggests that apoC-II monomers fold and self-assemble to form a stable cross-beta-scaffold containing relatively unstructured connecting loops. (unibas.ch)
  • Calcium(II) selectively induces alpha-synuclein annular oligomers via interaction with the C-terminal domain. (semanticscholar.org)
  • The ApoC-II binding site is currently unknown, but it is predicted that residues on both N-and C-terminal domains are necessary for this interaction to occur. (wikipedia.org)
  • Taken together, our results suggested that fatty acid recruitment from the circulation by apoC-II-activated LPL could be regionally controlled by modulation of apoC-II secretion [ 12 ] for the purpose of surfactant synthesis. (biomedcentral.com)
  • The amino acid sequences of two tryptic peptides derived from HPLC-purified heavier BRF-2 isoform were determined to be YLAIAPPIIK and ALYYLQIHPQELR. (nih.gov)
  • Examination of apoC-II fibrils using transmission electron microscopy, scanning transmission electron microscopy, and atomic force microscopy indicated that the fibrils are flat ribbons composed of one apoC-II molecule per 4.7-A rise of the cross-beta-structure. (unibas.ch)
  • Purification, primary structure, and antimicrobial activities of bovine apolipoprotein A-II. (ebi.ac.uk)
  • In this paper we report the isolation of two isoforms of BRF-2 by further purification using high-performance liquid chromatography. (nih.gov)
  • Accumulation of apoC-II in secretory granule-like structures was not systematically observed, but was found in the distal epithelium only at the end of gestation and soon after birth, mainly in epithelia with no or small lumina. (nih.gov)
  • Extracellular processing of proapolipoprotein A-II in Hep G2 cell cultures is mediated by a 54-kDa protease immunologically related to cathepsin B". The Journal of Biological Chemistry. (wikipedia.org)
  • The major site of apoC-II mRNA synthesis (positive signal, blue) changed after birth (compare A to C). Positive signals were found in newly-formed septa (D, E) and macrophages (E) on PN 5. (nih.gov)
  • We propose that BRF-2 exists both as a monomer (BRF-2M) and as a homooligomer. (nih.gov)
  • 22 PAF-AH hydrolyzes the acetyl moiety of the sn-2 position of PAF and also oxidized phospholipid with short-chain acyl moieties in the sn-2 position. (ahajournals.org)
  • We propose a model where apoC-II is retained in secretory granules in distal epithelial cells until the lumina reaches a minimum size, and is then secreted when the rate of surfactant production becomes optimal. (nih.gov)
  • In the Golgi apparatus, the oligosaccharides are further altered to result in either two complex chains, or two complex and one high-mannose chain. (wikipedia.org)
  • The plasma A-I/A-II weight ratio was 3.6±0.4 for men and 3.8±0.5 for women. (jci.org)
  • Cross-linking results using single-cysteine substitution mutants are consistent with a parallel in-register structural model for apoC-II fibrils. (unibas.ch)
  • Our structural model for apoC-II fibrils suggests that apoC-II monomers fold and self-assemble to form a stable cross-beta-scaffold containing relatively unstructured connecting loops. (unibas.ch)
  • To study apolipoprotein A-II, a simple, precise, and accurate immunodiffusion assay was developed and applied in a population sample of industrial employees. (jci.org)