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.
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.
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
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.
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.
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.
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.
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.
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 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.
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.
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.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
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
Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.
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.
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.
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.
Conditions with excess LIPIDS in the blood.
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.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
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).
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.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
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.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
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.
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.
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.
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
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).
A condition of elevated levels of TRIGLYCERIDES in the blood.
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.
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.
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 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.
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)
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 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.
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.
The main trunk of the systemic arteries.
A diet that contributes to the development and acceleration of ATHEROGENESIS.
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.
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.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
An individual having different alleles at one or more loci regarding a specific character.
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.
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.
A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
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.
An enzyme that catalyzes the deamination of cytidine, forming uridine. EC
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.
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.)
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 present in food, especially in animal products.
The rate dynamics in chemical or physical systems.
Pathological processes involving any part of the AORTA.
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.
Relating to the size of solids.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
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).
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.
The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.
A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.
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.
Lipid-laden macrophages originating from monocytes or from smooth muscle cells.
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)
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.
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.
An individual in which both alleles at a given locus are identical.
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
A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).
Transport proteins that carry specific substances in the blood or across cell membranes.
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.
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.
Diseases in which there is a familial pattern of AMYLOIDOSIS.
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)
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.
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.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
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
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.
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.
Established cell cultures that have the potential to propagate indefinitely.
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.
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.
A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.
Substances used to lower plasma CHOLESTEROL levels.
Proteins prepared by recombinant DNA technology.
Elements of limited time intervals, contributing to particular results or situations.
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.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
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 .
The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.
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.
Lesions formed within the walls of ARTERIES.
A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
Electrophoresis in which agar or agarose gel is used as the diffusion medium.
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.
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)
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).
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
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.
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.
The time frame after a meal or FOOD INTAKE.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The interstitial fluid that is in the LYMPHATIC SYSTEM.
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.
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.
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
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.
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.
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.
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.
An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.
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.
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 on non-ionic gels without regard to the mechanism of solute discrimination.
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.
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.
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).
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.
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.
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.
Genotypic differences observed among individuals in a population.
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.
Abstaining from all food.
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.
Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.
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 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.
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).
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.
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.
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).
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.
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.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
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.
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.
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)
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.
The dilatation of the aortic wall behind each of the cusps of the aortic valve.
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 bearing mutant genes which are phenotypically expressed in the animals.
Low-density subclass of the high-density lipoproteins, with particle sizes between 8 to 13 nm.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
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.
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.
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.
Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
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.
The sum of the weight of all the atoms in a molecule.
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.
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.
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.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Regular course of eating and drinking adopted by a person or animal.
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.
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.
7-carbon saturated monocarboxylic acids.
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 produced by a single clone of cells.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
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.
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.
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)
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.
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.
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.
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)
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 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.
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.
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)
Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor.
A human liver tumor cell line used to study a variety of liver-specific metabolic functions.

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)

Apolipoprotein A-II/ApoA2 Antibodies available through Novus Biologicals. Browse our Apolipoprotein A-II/ApoA2 Antibody catalog backed by our Guarantee+.
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:
Tsao YK, Wei CF, Robberson DL, Gotto AM, Chan L (Dec 1985). Isolation and characterization of the human apolipoprotein A-II gene. Electron microscopic analysis of RNA:DNA hybrids, nucleotide sequence, identification of a polymorphic MspI site, and general structural organization of apolipoprotein genes. The Journal of Biological Chemistry. 260 (28): 15222-31. PMID 2415515 ...
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 ...
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class=publication>Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href=>Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
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 ...
Sudo K, Takahashi E, Nakamura Y (Jan 1996). Isolation and mapping of the human EIF4A2 gene homologous to the murine protein synthesis initiation factor 4A-II gene Eif4a2. Cytogenet Cell Genet. 71 (4): 385-8. doi:10.1159/000134145. PMID 8521730 ...
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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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シクロデキストリン加アガロースゲル等電点電気泳動法によるヒト血清中のアポリポ蛋白AI, AIIの分画 (1995 ...
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...
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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 ...
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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. …
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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.
IMATI (,April 2015). Until April 2015 IMATI Reports are arranged into three collections, one for each Section. Click on the buttons below to retrieve the TR youre looking for! Pavia Genova Milano ...
Online Mendelian Inheritance in Man (OMIM): Apolipoprotein C-II Deficency - 207750 Yamamura T, Sudo H, Ishikawa K, Yamamoto A ( ... "Familial type I hyperlipoproteinemia caused by apolipoprotein C-II deficiency". Atherosclerosis. 34 (1): 53-65. doi:10.1016/ ... Hyperlipoproteinemia type II is further classified into types IIa and IIb, depending mainly on whether elevation in the ... The lipoprotein density and type of apolipoproteins it contains determines the fate of the particle and its influence on ...
August 1992). "Apolipoprotein AI mutation Arg-60 causes autosomal dominant amyloidosis". Proc. Natl. Acad. Sci. U.S.A. 89 (16 ... with congenital mutations in apolipoprotein A1 and lysozyme. It is also known as "Ostertag" type, after B. Ostertag, who ... 118 (3): 321-2. doi:10.1016/j.amjmed.2004.10.022. PMID 15745733. Granel B, Valleix S, Serratrice J, et al. (January 2006). " ... 20 (2): 444-51. doi:10.1681/ASN.2008060614. PMC 2637055. PMID 19073821. Uemichi T, Liepnieks JJ, Gertz MA, Benson MD (September ...
"Genetic studies of human apolipoproteins. XVIII. apolipoprotein polymorphisms in Australian Aborigines", Human Biology, 63 (2 ... ISBN 978-0-19-857695-2 Kamboh, M. I.; Serjeantson, Susan W.; Ferrell, R. E. (1991), " ...
... and therefore may tie the two conditions together. Anti-cardiolipin antibodies can be classified in two ways: As IgM, IgG or ... Only a subset of autoimmune anti-cardiolipin antibodies bind Apo-H, these anti-apolipoprotein antibodies are associated with ... In SLE, anti-DNA antibodies and anti-cardiolipin antibodies may be present individually or together; the two types of ... apolipoprotein H)". Proc. Natl. Acad. Sci. U.S.A. 87 (11): 4120-4124. Bibcode:1990PNAS...87.4120M. doi:10.1073/pnas.87.11.4120 ...
... sensitive and accurate screening of apolipoproteins and mutations of them. Apolipoproteins represent a groups of proteins with ... Nelson and colleagues did a study using MSIA to characterize and isolate apolipoproteins species.[citation needed] There are ... "Novel mass spectrometric immunoassays for the rapid structural characterization of plasma apolipoproteins". Journal of Lipid ... Tubbs, Kemmons A.; Nedelkov, Dobrin; Nelson, Randall W. (2001). "Detection and Quantification of β-2-Microglobulin Using Mass ...
The two positions are lightheartedly described as "ba-ptist" and "tau-ist" viewpoints in one scientific publication. Therein, ... 1997). "No difference in cerebral glucose metabolism in patients with Alzheimer disease and differing apolipoprotein E ... Two alternative misfolding hypotheses instead suggest that either tau protein or amyloid beta initiates the cascade. While ... Soluble intracellular (o)Aβ42 Two papers have shown that oligomeric (o)Aβ42 (a species of Aβ), in soluble intracellular form, ...
November 2005). "Variable expressivity of the clinical and biochemical phenotype associated with the apolipoprotein E p. ... 80 (10): 620-2. doi:10.1007/s002770100354. PMID 11732877. Suzuki O, Abe M (April 2007). "Secondary sea-blue histiocytosis ...
Hypothalamic-pituitary failure WHO group II of ovulation disorders: Hypothalamic-pituitary dysfunction. WHO group II is the ... intronic variant is significantly associated with decreased risk of Alzheimer's disease in males carrying an apolipoprotein E ... These two hormones play an important role in communicating to the gonads. In females FSH and LH act primarily to activate the ... Genetic mutations and chromosomal abnormalities are two sources of HPG axis alteration. Single mutations usually lead to ...
1998). "Characterization of two human genes encoding acyl coenzyme A:cholesterol acyltransferase-related enzymes". J. Biol. ... The enzyme is implicated in cholesterol absorption in the intestine and in the assembly and secretion of apolipoprotein B- ... 1996). "Sterol esterification in yeast: a two-gene process". Science. 272 (5266): 1353-6. Bibcode:1996Sci...272.1353Y. doi: ... Sterol O-acyltransferase 2, also known as SOAT2, is an enzyme that in humans is encoded by the SOAT2 gene. This gene is a ...
In some cases, drusen develop above the so-called pillars of the choriocapillaris that is the area between two micro vessels; ... The protein composition of drusen includes apolipoproteins and oxidized proteins, likely originating from blood, RPE, and ... 2 (2): 1-69. doi:10.1007/BF02720657. Lengyel I, Tufail A, Hosaini HA, Luthert P, Bird AC, Jeffery G (September 2004). " ... 1 (2): 106-18. doi:10.1007/BF02720791. Müller H (January 1856). "Anatomische Beiträge zur Ophthalmologie - Untersuchungen über ...
High-density lipoproteins are created when a protein in the bloodstream, Apolipoprotein A1 (apoA1), combines with cholesterol ... two copies of the gene must be present in the genotype. Most often, the parents of an individual with an autosomal recessive ...
Apolipoprotein L3 is a protein that in humans is encoded by the APOL3 gene. This gene is a member of the apolipoprotein L gene ... and two novel genes". Blood. 93 (10): 3418-31. PMID 10233894. Dunham I, Shimizu N, Roe BA, et al. (1999). "The DNA sequence of ... "Entrez Gene: APOL3 apolipoprotein L, 3". Human APOL3 genome location and APOL3 gene details page in the UCSC Genome Browser. ... 2001). "Apolipoprotein L gene family: tissue-specific expression, splicing, promoter regions; discovery of a new gene". J. ...
Dabbing Syndrome Defect in synthesis of adenosylcobalamin Defective apolipoprotein B-100 Defective expression of HLA class 2 ... nephrogenic type 2 Diabetes insipidus, nephrogenic type 3 Diabetes insipidus, nephrogenic, dominant type Diabetes insipidus, ... congenital type 2 Dyserythropoietic anemia, congenital type 3 Dysferlinopathy Dysfibrinogenemia, familial Dysfibrinogenemia, ... nephrogenic, recessive type Diabetes mellitus Diabetes mellitus type 1 Diabetes mellitus type 2 Diabetes persistent mullerian ...
By using these two methods, the researchers were able to overcome the criticism that candidate gene studies are solely focused ... apolipoprotein C3 gene) that associated with higher risks of hypertriglyceridemia and atherosclerosis. In a study by Kim et al ... Lynx provides two sophisticated prioritization tools, Cheetoh and PINTA, to help users select candidate genes from the whole ... 2 (12): 16179. doi:10.1038/nplants.2016.179. ISSN 2055-0278. PMC 5131878. PMID 27892923. Gene Gene Ontology Consortium Topp ...
Two of the genes associated with most aggressive forms of Alzheimer's disease, namely presenilin 1 and presenilin 2, which are ... The association of late-onset Alzheimer's disease with the Epsilon 4 allele of apolipoprotein E was co-discovered there in ...
Apolipoprotein E are proteins that metabolize fats in the body. In studies of patients undergoing coronary artery bypass ... NGAL is secreted at high levels in the blood and urine within two hours of injury. IMA- Ischemic Modified Albumin. IMA can be ... Genes such as Apolipoprotein E (APO E), which controls cholesterol metabolism, NADPH Oxidase which regulates oxidative stress, ... These are proapoptotic genes that can be categorized in two: extrinsic and intrinsic pathways. The extrinsic pathway are ...
These tests must be carried out on a minimum of two occasions at least 6 weeks apart and be positive on each occasion, ... anti-apolipoprotein antibodies, or anti-cardiolipin antibodies. Antiphospholipid syndrome can be primary or secondary. Primary ... The diagnostic criteria require one clinical event (i.e. thrombosis or pregnancy complication) and two positive blood test ... This is tested for by using a minimum of two coagulation tests that are phospholipid-sensitive, due to the heterogeneous nature ...
Two of the most prevalent deaminase reactions occur through the Apolipoprotein B mRNA editing enzyme (APOBEC) and the adenosine ... Missense mRNAs may be detected as a result of two different types of point mutations - spontaneous mutations and induced ... Nucleoside analogues such as 2-aminopurine and 5-bromouracil can insert in place of A and T respectively. Ionizing radiation ...
The apolipoproteins are produced by the secretory pathway in type II cells. They undergo much post-translational modification, ... Half of this 10% is plasma proteins but the rest is formed by the apolipoproteins, surfactant proteins SP-A, SP-B, SP-C, and SP ... It can be both broken down by macrophages and/or reabsorbed into the lamellar structures of type II pneumocytes. Up to 90% of ... Surfactant immune function is primarily attributed to two proteins: SP-A and SP-D. These proteins can bind to sugars on the ...
... class II, DP alpha 1 Major histocompatibility complex, class II, DQ alpha 1 Myosin light chain A1, an actin-binding protein ... member A1 Alpha-1-microglobulin/bikunin precursor Apolipoprotein A1 and ApoA-1 Milano ATPase, H+ transporting, lysosomal V0 ... type II, alpha 1 Collagen, type III, alpha 1 Collagen, type IV, alpha 1 Collagen, type V, alpha 1 Collagen, type VI, alpha 1 ... alpha 1 Adaptor-related protein complex 2, alpha 1 Aldehyde dehydrogenase 3 family, member A1 Aldehyde dehydrogenase 4 family, ...
She has also generated a HIV/SIV Viral infectivity factor (Vif)-APOlipoprotein B mRNA-Editing Catalytic polypeptide (APOBEC) ... 2 (4): 269-276. doi:10.1038/nmeth746. ISSN 1548-7105. PMID 15782219. Simon, V R; Swayne, T C; Pon, L A (1995-07-15). "Actin- ... 130 (2): 345-354. doi:10.1083/jcb.130.2.345. ISSN 0021-9525. PMC 2199926. PMID 7615636. Simon, Viviana (1998). Methodische ... is active against HIV-1 and HIV-2, as well as LTR retrotransposon and Hepatitis B. Simon has demonstrated that the HIV Viral ...
... apolipoprotein C is a family of four low molecular weight apolipoproteins, designated as C-I, C-II, C-III, and C-IV that are ... In the fasting state, the C apolipoproteins are mainly associated with HDL. During absorption of dietary fat, the C ... Mahley RW, Innerarity TL, Rall SC, Weisgraber KH (December 1984). "Plasma lipoproteins: apolipoprotein structure and function ... apolipoproteins preferentially redistribute to the surface of the triglyceride-rich chylomicrons and VLDL. ...
These two activities can be differentiated by the binding to Apo-H domains, whereas binding to the 5th domain promotes that ... 2000). "HLA class II alleles associations of anticardiolipin and anti-beta2GPI antibodies in a large series of European ... In autoimmune disease, anti-apolipoprotein H (AAHA) antibodies, also called anti-β2 glycoprotein I antibodies, comprise a ... 70 (2): 342-5. doi:10.1055/s-0038-1649577. PMID 8236146. Schousboe I, Rasmussen MS (1995). "Synchronized inhibition of the ...
Cornelius C, Fastbom J, Winblad B, Viitanen M (2004). "Aspirin, NSAIDs, risk of dementia, and influence of the apolipoprotein E ... Retrieved 2 October 2009. Peters R, Beckett N, Forette F, Tuomilehto J, Clarke R, Ritchie C, et al. (August 2008). "Incident ... Retrieved 2 October 2009. Alladi S, Bak TH, Duggirala V, Surampudi B, Shailaja M, Shukla AK, et al. (November 2013). " ... 10 (2): 179-186. doi:10.1016/j.jalz.2013.03.002. PMC 3783589. PMID 23706517. Livingston G, Sommerlad A, Orgeta V, Costafreda SG ...
Given the frequency of GC two-nucleotide sequences, the number of CpG dinucleotides is much lower than would be expected. A ... 5hmC can be oxidatively deaminated by activity-induced cytidine deaminase/apolipoprotein B mRNA editing complex (AID/APOBEC) ... On the other hand, the promoters of two genes, PARP1 and FEN1, were hypomethylated and these genes were over-expressed in ... Saxonov S, Berg P, Brutlag DL (2006). "A genome-wide analysis of CpG dinucleotides in the human genome distinguishes two ...
"Microarray analysis of colorectal cancer stromal tissue reveals upregulation of two oncogenic miRNA clusters". Clinical Cancer ... "Derepression of microRNA-mediated protein translation inhibition by apolipoprotein B mRNA-editing enzyme catalytic polypeptide- ... 32 (2): 242-50. doi:10.1038/onc.2012.32. PMID 22349819. Hu Z, Dong J, Wang LE, Ma H, Liu J, Zhao Y, Tang J, Chen X, Dai J, Wei ... 56 (2): 211-6. doi:10.1002/pbc.22723. PMID 21157891. Li LM, Hu ZB, Zhou ZX, Chen X, Liu FY, Zhang JF, Shen HB, Zhang CY, Zen K ...
RNA polymerase II regulatory region sequence-specific DNA binding. • RNA polymerase II transcription factor activity, ligand- ... "Farnesoid X receptor agonists suppress hepatic apolipoprotein CIII expression". Gastroenterology. 125 (2): 544-55. doi:10.1016/ ... RNA polymerase II distal enhancer sequence-specific DNA binding. • sequence-specific DNA binding. • DNA binding. • ... RNA polymerase II transcription factor activity, sequence-specific DNA binding. Cellular component. • nuclear euchromatin. • ...
Females typically have two X chromosomes, whereas males typically have one X and one Y chromosome. Both males and females ... AD16: encoding Alzheimer disease 16 protein AIC: encoding protein AIC APOO: encoding protein Apolipoprotein O ARMCX6: encoding ... Males with Klinefelter syndrome typically have one extra copy of the X chromosome in each cell, for a total of two X ... It is entirely coincidental that the Y chromosome, during mitosis, has two very short branches which can look merged under the ...
These molecules contain apolipoprotein B100 and apolipoprotein E in their shells, and can be degraded by lipoprotein lipase on ... Two molecules of farnesyl pyrophosphate then condense to form squalene by the action of squalene synthase in the endoplasmic ... Chylomicrons, the least dense cholesterol transport molecules, contain apolipoprotein B-48, apolipoprotein C, and ... adjusted for apolipoprotein A-I and apolipoprotein B) and increased risk of cardiovascular disease, casting doubt on the ...
... and apolipoprotein B (apo B), and to increase high-density lipoprotein cholesterol (HDL) in adults with primary ... whereas their effect on HDL metabolism is associated with changes in HDL apolipoprotein expression." Fenofibrate is a fibric ... 4 (2): 47-55. doi:10.4021/cr270w. PMC 5358213. PMID 28352420. Alagona P (2010). "Fenofibric acid: a new fibrate approved for ... Steiner G (2009). "How can we improve the management of vascular risk in type 2 diabetes: insights from FIELD". Cardiovasc ...
2002). "Regulated expression of the apolipoprotein E/C-I/C-IV/C-II gene cluster in murine and human macrophages. A critical ... Apolipoprotein C-IV, also known as apolipoprotein C4, is a protein that in humans is encoded by the APOC4 gene.[5][6] ... Apolipoprotein (apo)C4 gene is a member of the apolipoprotein C gene family. It is expressed in the liver and has a predicted ... in the apolipoprotein E, C-I, and C-II gene locus". Genomics. 28 (2): 291-300. doi:10.1006/geno.1995.1144. PMID 8530039.. ...
Aktivin i inhibin • ADAM • Alfa 1-antihimotripsin • Apolipoprotein H • CD70 • Asijaloglikoprotein • Avidin • B-ćelijski ... proinflamatorni citokin (IL-1, TNF-alfa) • Th1 (INF-gama i TNF-beta) • Th2 (IL-4, IL-5, IL-6, IL-10, IL-13) • Th17 (IL-17,IL-22 ... CD201 • CD202b • CD204 • CD205 • CD206 • CD207 • CD208 • CD209 • CDw210 (a, b) • CD212 • CD213a (1, 2) • CD217 • CD218 (a, b) ... 2]. Faktor aktivacije B-ćelija, (BAFF) koji je takođe poznat kao faktor nekroze tumora ligand superfamilija član 13B, je ...
Munger KL, Chitnis T, Ascherio A. Body size and risk of MS in two cohorts of US women. Neurology (Comparative Study). 2009, 73 ... 載脂蛋白B缺乏症(英语:Apolipoprotein B deficiency) ... 磷酸酯 · 三聚氰胺(美耐皿) · 酸酐 · 順丁烯二酸酐 · 順丁烯二酸 · 己二酸鹽(英语:Adipate)(己二酸二(2 ... 肥胖會增加心血管
... adjusted for apolipoprotein A-I and apolipoprotein B) and increased risk of cardiovascular disease, casting doubt on the ... two enzymes that are activated by SCAP when cholesterol levels are low. The cleaved SREBP then migrates to the nucleus and acts ... By serving as ligands for specific receptors on cell membranes, the apolipoproteins that reside on the surface of a given ... van der Steeg WA (2008). "High-density lipoprotein cholesterol, high-density lipoprotein particle size, and apolipoprotein A-I ...
Apolipoprotein BEdit. Apolipoprotein B, in its ApoB100 form, is the main apolipoprotein, or protein part of the lipoprotein ... Class II: LDLR is not properly transported from the endoplasmic reticulum to the Golgi apparatus for expression on the cell ... 2 (72): 171-76. doi:10.1016/0002-9149(93)90155-6.. *^ a b c d e f g h i Repas TB, Tanner JR (February 2014). "Preventing early ... Having two abnormal copies (being homozygous) may cause severe cardiovascular disease in childhood. Heterozygous FH is a common ...
APOA4: apolipoprotein A-IV. *ATM: ataxia telangiectasia mutated (includes complementation groups A, C and D) ...
Sodium phenylbutyrate phase II human triasl with 12 to 15 g/day showed restored mRNA levels of Htt mutant repressed genes but ... and familial inheritance of apolipoprotein E allele epsilon 4. In addition to these common factors, there are a number of other ... Class I and II HDAC inhibitors such as trichostatin A, vorinostat, and sodium butyrate, and Class III HDACis, such as ... Sodium butyrate is a class I and II HDACi and has been shown to recover learning and memory after 4 weeks,[13] decrease ...
Hargraves M, Richmond H, Morton R. Presentation of two bone marrow components, the tart cell and the LE cell. Mayo Clin Proc ... a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap Table 6-2 in: Elizabeth D ... There are two speckled patterns: fine and coarse. The fine speckled pattern has fine nuclear staining with unstained metaphase ... doi:10.7326/0003-4819-140-2-200401200-00013. PMID 14706971.. *^ a b c Ho, KT; Reveille, JD (2003). "The clinical relevance of ...
2009). "Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip". Am. J. Hum. ... 57 (2): 283-92. doi:10.1016/j.eururo.2009.08.001. PMC 3220186 . PMID 19692168. Lin JC, Kuo WR, Chiang FY, et al. (2009). " ... 36 (2): 405-14. doi:10.3892/ijo_00000513. PMID 20043075. Chung SS, Kim M, Youn BS, et al. (2009). "Glutathione peroxidase 3 ... 66 (2): 96-8. doi:10.1159/000133675. PMID 8287691. Guey LT, García-Closas M, Murta-Nascimento C, et al. (2010). "Genetic ...
It was recently shown that bacteria also have a sort of 5' cap consisting of a triphosphate on the 5' end.[24] Removal of two ... An example in humans is the apolipoprotein B mRNA, which is edited in some tissues, but not others. The editing creates an ... This process of translation of codons into amino acids requires two other types of RNA: Transfer RNA (tRNA), that mediates ... 2 (10): 17056. doi:10.1038/natrevmats.2017.56.. *^ a b Gousseinov, Elina; Kozlov, Mikhail; Scanlan, Claire; Hammons, Aaron; Bei ...
1997). „Signaling of type II oncostatin M receptor.". J. Biol. Chem. 272 (25): 15760-4. PMID 9188471. doi:10.1074/jbc.272.25. ... Aktivin i inhibin • ADAM • Alfa 1-antihimotripsin • Apolipoprotein H • CD70 • Asijaloglikoprotein • Avidin • B-ćelijski ... 2]. Glikoprotein 130 (takođe poznat kao gp130, IL6ST, IL6-beta ili CD130) je transmembranski protein. On je osnivački član ... CD201 • CD202b • CD204 • CD205 • CD206 • CD207 • CD208 • CD209 • CDw210 (a, b) • CD212 • CD213a (1, 2) • CD217 • CD218 (a, b ...
ApoA-II. structures of apolipoprotein a-ii and a lipid surrogate complex provide insights into apolipoprotein-lipid ... 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 ... Apolipoprotein A-II is a protein that in humans is encoded by the APOA2 gene.[5] ...
... of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins ... of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins ... Soluble in alcohols, (C2H5)2O, phenyls, haloalkanes, acetates[4] ...
APOE: Apolipoprotein E, gene associated with Alzheimer's disease. *BCKDHA: Branched chain keto acid dehydrogenase E1, alpha ... at kumakatawan sa pagitan ng 2 at 2.5% ng kabuuang DNA sa selula. Ang pagtukoy sa mga gene sa bawat kromosoma ay isang aktibong ...
... two in pairs), two world titles, and the 1992 Olympic gold medal in singles figure skating. Rena Inoue, a Japanese immigrant to ... Specifically too, the apolipoprotein *e4 allele is linked to Alzheimer's disease as well. Also, there is increased coronary ... and was a multiple national champion and an Olympian with two different partners. Two-time Olympian Mirai Nagasu won the 2008 U ... "The War Relocation Centers of World War II: When Fear Was Stronger than Justice", a National Park Service Teaching with ...
Apolipoproteins. *Growth factors. *Chemokines. The enzymes and proteins listed above serve to reinforce the glycocalyx barrier ... 2] The glycocalyx plays a major role in regulation of endothelial vascular tissue, including the modulation of red blood cell ...
"II. THE PROKARYOTIC CELL: BACTERIA". Retrieved 1 May 2011.. *^ a b c d e f g h White, D. (2007). The physiology and ... In step two, an acetyl group is transferred from acetyl CoA to the amino group on the glucosamine-6-phosphate creating N-acetyl ... Stage two occurs in the cytoplasmic membrane. It is in the membrane where a lipid carrier called bactoprenol carries ... The peptidoglycan layer in the bacterial cell wall is a crystal lattice structure formed from linear chains of two alternating ...
In 2015 a randomized, two-period crossover human study, showed that EPA and DHA from oil extracted from the small crustacean ... and astaxanthin-rich extract from the marine copepod Calanus finmarchicus attenuates atherogenesis in female apolipoprotein E- ... "Amer Zool (2). doi:10.1093/icb/38.2.321.. *^ Bledsoe, G.E. (2003). "Caviars and fish roe products". Crit Rev Food Sci Nutr. 43 ... 2. O. {\displaystyle {\ce {RCOOH + R'OH ,=, RCOOR' + H2O}}}. Various types of wax esters exist. Some are saturated, and others ...
This region is called the Fc (Fragment, crystallizable) region, and is composed of two heavy chains that contribute two or ... The Ig monomer is a "Y"-shaped molecule that consists of four polypeptide chains; two identical heavy chains and two identical ... They are typically made of basic structural units-each with two large heavy chains and two small light chains. There are ... Several immunoglobulin domains make up the two heavy chains (red and blue) and the two light chains (green and yellow) of an ...
... the doctor had collected thirty-two cases. Sixteen of them were born to women taking primidone. 25% of the thirty-two cases had ... and apolipoproteins A and B.[24] ... two adult survivors ingested 30 g[46] 25 g,[51] and 22.5 g.[47] ... or within two weeks of stopping any one of them may potentiate the effects of primidone or change one's seizure patterns.[54] ... 12 (2): 183-8. PMID 13403983.. *^ a b c Kidd, Patrick; David L. Mollin (October 26, 1957). "Megaloblastic Anaemia and Vitamin- ...
Two other naturally occurring 13-HODEs that may accompany the production of 13(S)-HODE are its cis-trans (i.e., 9E,11E) isomers ... "Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis". Nature ... Other studies have lumped together the 9-(S), 9(R), 13 (S)-, and 13(R)-HODEs along with the two ketone metabolites of these ... 18 (2): 349-56. doi:10.1021/tx049685x. PMID 15720142.. *^ a b c d Yoshida, Yasukazu; Umeno, Aya; Akazawa, Yoko; Shichiri, ...
"Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip". American Journal of ... "Spred1 and TESK1--two new interaction partners of the kinase MARKK/TAO1 that link the microtubule and actin cytoskeleton" ... Lock P, I ST, Straffon AF, Schieb H, Hovens CM, Stylli SS (December 2006). "Spred-2 steady-state levels are regulated by ... 2 Frameshift (c.1048_c1049 delGG, c.149_1152del 4 bp)[9] ...
Nussenzveig DR, Mathew S, Gershengorn MC (1995). "Alternative splicing of a 48-nucleotide exon generates two isoforms of the ... Zhang, Jianying; Herscovitz Haya (February 2003). "Nascent lipidated apolipoprotein B is transported to the Golgi as an ... Linnik, K M; Herscovitz H (August 1998). "Multiple molecular chaperones interact with apolipoprotein B during its maturation. ... The network of endoplasmic reticulum-resident chaperones (ERp72, GRP94, calreticulin, and BiP) interacts with apolipoprotein b ...
APOA4: Apolipoprotein A-IV. *Ataksijska telangiektazija,mutirana ATM (uključujući kkomplementacijske grupe A, C i D) ...
"Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis". Nat. ... 2: 7. doi:10.1186/1471-2156-2-7. PMC 31346. PMID 11299043.. الوسيط ,CitationClass=. تم تجاهله (مساعدة). ... FABP2‏ (Fatty acid binding protein 2) هوَ بروتين يُشَفر بواسطة جين FABP2 في الإنسان.[1] ... 12 (2): 241-53. doi:10.1016/0888-7543(92)90371-X. PMID 1740333.. الوسيط ,CitationClass=. تم تجاهله (مساعدة). ...
apolipoprotein A-I receptor binding. • GTP-dependent protein binding. • GTPase activity. • mitogen-activated protein kinase ... Stewart II, Kuehl B, Hogue K, Colwill K, Gladwish K, Muskat B, Kinach R, Adams SL, Moran MF, Morin GB, Topaloglou T, Figeys D ( ... 46 (2): 757-63. doi:10.3892/ijo.2014.2748. PMID 25394485.. *^ a b c d e Wilson JM, Menkhaus P, Gustin BW (May 1987). "Volume ... 2 (8): 531-9. doi:10.1038/35019573. PMID 10934474.. *^ a b Noda Y, Takeya R, Ohno S, Naito S, Ito T, Sumimoto H (February 2001 ...
The apolipoproteins forming the surface of the given lipoprotein particle determine from what cells cholesterol will be removed ... 37 (2): 49-52. PMID 1609267.. *^ Dobson, HM; Muir, MM; Hume, R (1984). "The effect of ascorbic acid on the seasonal variations ...
74.0 74.1 Mahley RW, Weisgraber KH, Huang Y (Aprili 2006). "Apolipoprotein E4: a causative factor and therapeutic target in ... Shen ZX (2004). "Brain cholinesterases: II. The molecular and cellular basis of Alzheimer's disease". Med Hypotheses 63 (2): ... Polvikoski T, Sulkava R, Haltia M, et al. (Novemba 1995). "Apolipoprotein E, dementia, and cortical deposition of beta-amyloid ... Strittmatter WJ, Saunders AM, Schmechel D, et al. (Machi 1993). "Apolipoprotein E: high-avidity binding to beta-amyloid and ...
Apolipoprotein A-II. Apolipoprotein A-II, Apo-AII, ApoA-II (Apolipoprotein A2) [Cleaved into: Proapolipoprotein A-II, ProapoA- ... Apolipoprotein A-IIARBA annotation. ,p>Information which has been generated by the UniProtKB automatic annotation system, ... Apolipoprotein A-IISequence analysis. Automatic assertion according to sequence analysisi ... tr,V9GYS1,V9GYS1_HUMAN Apolipoprotein A-II OS=Homo sapiens OX=9606 GN=APOA2 PE=1 SV=1 ...
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. ...
Human Apolipoprotein AII Purification: Affinity purified Buffer: 75 mM Sodium Phosphate, 75 mM NaCl, 0.5 mM EDTA, 0.02% NaN3, ... "Amino Acid Sequence of Human ApoLp-Gln-II (apoA-II), an Apolipoprotein Isolated from the High-Density Lipoprotein Complex." ... "Apolipoprotein A-II Is Inversely Associated With Risk of Future Coronary Artery Disease." Circulation 116 (2007): 2029-035. ... 2016): Posttranslational modifications of apolipoprotein A-II proteoforms in type 2 diabetes. In Journal of Clinical Lipidology ...
ApoA-II. structures of apolipoprotein a-ii and a lipid surrogate complex provide insights into apolipoprotein-lipid ... 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 ... Apolipoprotein A-II is a protein that in humans is encoded by the APOA2 gene.[5] ...
When a sample that has an apolipoprotein AII concentration around 30 mg/dL is assayed 20 times (within-run), the absorbance C.V ... For the quantitative determination of human Apolipoprotein AII (Apo AII) in serum and plasma by immunoturbidimetric assay. FOR ... Reagent-2 (R-2) Click here for information about recommended calibrators and controls.. ... All reagents should be stored refrigerated (2-8°C). Return all reagents to 2-8°C promptly after use. Unopened reagents can be ...
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, ...
Anti-Apolipoprotein A II antibody conjugated to Biotin validated for WB, ELISA and tested in Human. Immunogen corresponding to ... Anti-Apolipoprotein A II antibody (Biotin). See all Apolipoprotein A II primary antibodies. ... The antibody can be used for detection of human Apolipoprotein A II in plasma and lipoproteins, immunoassays and immunoblots. ... Shipped at 4°C. Store at +4°C short term (1-2 weeks). Store at -20°C or -80°C. Avoid freeze / thaw cycle. ...
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. ...
Absence of CC chemokine receptor-2 reduces atherosclerosis in apolipoprotein E-deficient mice.. Dawson TC1, Kuziel WA, Osahar ...
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. ...
Tags: Randox Reagents, lipids, apolipoprotein, cardiac, Apo C-II, Apolipoprotein C-II, triglyceride, hypertriglyceridemia, ... Apolipoprotein C-II (Apo C-II) Assay. Posted on 1st October 2020 at 9:00 am.. Written by Randox Communications ... Structure of a biologically active fragment of human serum apolipoprotein C-II in the presence of sodium dodecyl sulfate and ... A review of the role of apolipoprotein C-II in lipoprotein metabolism and cardiovascular disease. Metabolism: Clinical and ...
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- ...
Browse our Apolipoprotein A-II/ApoA2 Antibody catalog backed by our Guarantee+. ... Apolipoprotein A-II/ApoA2 Antibodies available through Novus Biologicals. ... Alternate Names for Apolipoprotein A-II/ApoA2 Antibodies. anti-Apolipoprotein A-II/ApoA2 antibody, anti-APOA2 antibody, anti- ... Apolipoprotein A-II/ApoA2 Antibodies. We offer Apolipoprotein A-II/ApoA2 Antibodies for use in common research applications: ...
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 ...
Lipoprotein(a), Apolipoprotein(a) Polymorphism, and Insulin Treatment in Type II Diabetic Patients. ... Lipoprotein(a), Apolipoprotein(a) Polymorphism, and Insulin Treatment in Type II Diabetic Patients ... Lipoprotein(a), Apolipoprotein(a) Polymorphism, and Insulin Treatment in Type II Diabetic Patients ... Lipoprotein(a), Apolipoprotein(a) Polymorphism, and Insulin Treatment in Type II Diabetic Patients ...
Compare apolipoprotein B mRNA editing enzyme catalytic subunit 2 ELISA Kits from leading suppliers on Biocompare. View ... apolipoprotein B mRNA editing enzyme catalytic subunit 2 ELISA Kits. The ELISA (enzyme-linked immunosorbent assay) is a widely ... Human Apolipoprotein B mRNA Editing Enzyme Catalytic Subunit 2 (APOBEC2) ELISA Kit ... Your search returned 1 apolipoprotein B mRNA editing enzyme catalytic subunit 2 ELISA ELISA Kit across 1 supplier. ...
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 ...
Apolipoprotein E Polymorphism and Renal Function in German Type 1 and Type 2 Diabetic Patients. ... Apolipoprotein E Polymorphism and Renal Function in German Type 1 and Type 2 Diabetic Patients ... Apolipoprotein E Polymorphism and Renal Function in German Type 1 and Type 2 Diabetic Patients ... Apolipoprotein E Polymorphism and Renal Function in German Type 1 and Type 2 Diabetic Patients ...
Apolipoprotein A-II (A-II) did not increase with age in men (r = −0.20, n = 172), but showed a slight increase with age in ... To study apolipoprotein A-II, a simple, precise, and accurate immunodiffusion assay was developed and applied in a population ... The Measurement of Apolipoprotein A-I and A-II Levels in Men and Women by Immunoassay. ... The Measurement of Apolipoprotein A-I and A-II Levels in Men and Women by Immunoassay. ...
Genetic variation in the apolipoprotein H (beta2-glycoprotein I) gene affects plasma apolipoprotein H concentrations. Mehdi, H ... A hydrophobic sequence at position 313-316 (Leu-Ala-Phe-Trp) in the fifth domain of apolipoprotein H (beta2-glycoprotein I) is ... Genetic polymorphisms of apolipoproteins A-IV, E and H in Koreans. Kim, H.S., Kamboh, M.I. Hum. Hered. (1998) [Pubmed] ... Assignment of apolipoprotein H (APOH: beta-2-glycoprotein I) to human chromosome 17q23----qter; determination of the major ...
These two peptides were found to share 100% sequence homology with human hepatitis B virus X associated protein-1 (XAP-1) and ... Apolipoprotein B gene regulatory factor-2 (BRF-2) is structurally and immunologically highly related to hepatitis B virus X ... Hepatic cell-specific expression of the human apolipoprotein B (apoB) gene is controlled by at least four cis-acting elements ... 12, 3183-3191]. In this paper we report the isolation of two isoforms of BRF-2 by further purification using high-performance ...
RDN promoted atherosclerosis in apolipoprotein E-deficient mice infused with angiotensin II associated with upregulation of MMP ... RDN decreased systolic blood pressure in apolipoprotein E-deficient mice. Mice that had RDN had more severe aortic arch ... RDN decreased systolic blood pressure in apolipoprotein E-deficient mice. Mice that had RDN had more severe aortic arch ... Methods: Hypertension, atherosclerosis and aortic aneurysm were induced by subcutaneous infusion of angiotensin II (1 µg/kg/min ...
Identification of apolipoprotein D, apolipoprotein A-IV, apolipoprotein E, and apolipoprotein A-I. J Biol Chem 265:17805-17815. ... Two Distal Downstream Enhancers Direct Expression of the Human Apolipoprotein E Gene to Astrocytes in the Brain. Sharon Grehan ... 1995a) Identification and characterization of a new human gene (APOC4) in the apolipoprotein E, C-I, and C-II gene locus. ... Two distal downstream enhancers controlling astrocyte expression of the human apolipoprotein E (apoE) gene in the brain were ...
Targeted mass spectrometric immunoassays toward apolipoproteins A-I, A-II, and C-III were applied on large cross-sectional and ... Several correlations were observed, including greater apolipoprotein A-I and A-II oxidation in patients with diabetes and ... Reviewed here are recent studies correlating apolipoproteins proteoforms with the specific clinical measures of lipid ... Apolipoproteins function as structural components of lipoprotein particles, cofactors for enzymes, and ligands for cell-surface ...
HealthDay)-Apolipoprotein (apo) CIII and apoCIII-to-apoA1 ratio are correlated with incident type 2 diabetes (T2D), according ... HealthDay)-Apolipoprotein (apo) CIII and apoCIII-to-apoA1 ratio are correlated with incident type 2 diabetes (T2D), according ... and apoE and the ratios of apolipoproteins with apoA1 with T2D risk. ... ...
VLDL and apolipoprotein CIII induce ER stress and inflammation and attenuate insulin signalling via Toll-like receptor 2 in ... Åvall K, Ali Y, Leibiger IB et al (2015) Apolipoprotein CIII links islet insulin resistance to β-cell failure in diabetes. Proc ... Hiukka A, Fruchart-Najib J, Leinonen E, Hilden H, Fruchart JC, Taskinen MR (2005) Alterations of lipids and apolipoprotein CIII ... Aalto-Setälä K, Fisher EA, Chen X et al (1992) Mechanism of hypertriglyceridemia in human apolipoprotein (apo) CIII transgenic ...
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. ...
Sialidase Activity Acting on Apolipoprotein CIII 1 and 2 in Human Leukocytes and Platelets C H Bolton C H Bolton ... C H Bolton, A P Corfield, L G Downs; Sialidase Activity Acting on Apolipoprotein CIII 1 and 2 in Human Leukocytes and Platelets ... Study of DNA polymorphisms of the apolipoprotein AI-CIII-AIV gene cluster in patients with peripheral arterial disease Clin Sci ... DDAH-2 alleviates contrast medium iopromide-induced acute kidney injury through nitric oxide synthase ...
2) was more effective in inhibiting lesions than mR18L, possibly due to its ability to promote the secretion of apoE from ... Two apolipoprotein E mimetic peptides with similar cholesterol reducing properties exhibit differential atheroprotective ... Objective: We investigated two apoE mimetic peptides with similar long-term plasma cholesterol reducing abilities for their ... Epub 2012 Nov 2. Authors Shaila P Handattu 1 , Gaurav Nayyar, David W Garber, Mayakonda N Palgunachari, Candyce E Monroe, ...
Effect of atorvastatin on apolipoprotein B100 containing lipoprotein metabolism in type 2 diabetes. Khadija Ouguerram, Thierry ... Effect of atorvastatin on apolipoprotein B100 containing lipoprotein metabolism in type 2 diabetes. Khadija Ouguerram, Thierry ... Effect of atorvastatin on apolipoprotein B100 containing lipoprotein metabolism in type 2 diabetes. Khadija Ouguerram, Thierry ... Effect of atorvastatin on apolipoprotein B100 containing lipoprotein metabolism in type 2 diabetes ...
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 ...
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. ...
A-II HDL) and both apoA-I and apoA-II (A-I/A-II HDL). When lipid-free apoA-II was incubated with either VLDLs and lipoprotein ... Formation of apolipoprotein-specific high-density lipoprotein particles from lipid-free apolipoproteins A-I and A-II Moira A. ... Formation of apolipoprotein-specific high-density lipoprotein particles from lipid-free apolipoproteins A-I and A-II. Biochem J ... When both lipid-free apoA-I and lipid-free apoA-II were incubated with LDL and sodium oleate, both apolipoproteins were ...
  • Apolipoprotein A-II is a protein that in humans is encoded by the APOA2 gene . (
  • This gene encodes apolipoprotein (apo-) A-II, which is the second most abundant protein of the high density lipoprotein particles. (
  • The protein is found in plasma as a monomer, homodimer, or heterodimer with apolipoprotein D. Defects in this gene may result in apolipoprotein A-II deficiency or hypercholesterolemia. (
  • Binding of phospholipid transfer protein (PLTP) to apolipoproteins A-I and A-II: location of a PLTP binding domain in the amino terminal region of apoA-I". Journal of Lipid Research . (
  • Amino Acid Sequence of Human ApoLp-Gln-II (apoA-II), an Apolipoprotein Isolated from the High-Density Lipoprotein Complex. (
  • It exists in human plasma as a dimer of 2 identical chains of 77 amino acid residues, joined by disulfide. (
  • Comparison of the human apolipoprotein genes. (
  • Pownall, Henry J. (2017): Scavenger receptor B1 (SR-B1) profoundly excludes high density lipoprotein (HDL) apolipoprotein AII as it nibbles HDL-cholesteryl ester. (
  • 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 . (
  • This study was designed to investigate whether RDN affects atherosclerosis severity in hypertensive ApoE −/− mice infused with angiotensin II. (
  • Two distal downstream enhancers controlling astrocyte expression of the human apolipoprotein E (apoE) gene in the brain were identified by analysis of transgenic mice generated with various constructs of the apoE/C-I/C-IV/C-II gene cluster. (
  • Expression of the human apoE transgene at these sites was specified by two enhancer domains: one enhancer is located 3.3 kb downstream of the apoE gene, and a duplication of this sequence is located 15 kb downstream of the apoE gene. (
  • The localization of the two astrocytic enhancers reveals an unexpected complexity in the control of apoE production that is essential to understanding apoE function in the brain. (
  • Apolipoprotein E (apoE) is a protein ( M r = 35,000) that functions in the CNS. (
  • They examined the correlation of high-density lipoprotein cholesterol (HDL-C), apoA1, apoCIII, apoD, and apoE and the ratios of apolipoproteins with apoA1 with T2D risk. (
  • We investigated two apoE mimetic peptides with similar long-term plasma cholesterol reducing abilities for their effects on atherosclerotic lesions in Western diet-fed female LDL-receptor (LDL-R) null mice. (
  • Incubation of HepG2 cells and THP-1 monocyte-derived macrophages with both peptides in the presence of oxidized phospholipid showed that Ac-hE18A-NH(2) promotes the secretion of apoE from the cells whereas mR18L does not. (
  • Despite similar reductions in plasma cholesterol levels, Ac-hE18A-NH(2) was more effective in inhibiting lesions than mR18L, possibly due to its ability to promote the secretion of apoE from hepatocytes and macrophages. (
  • Induction of T helper 2 responses against human Apolipoprotein B100 does not affect atherosclerosis in ApoE-/- mice. (
  • APOE genotypes and allele distribution were ascertained in a blinded manner from frozen samples (2% with ε 2/ε 2, 9% with ε 2/ε 3, 1% with ε 2/ε 4, 71% with ε 3/ε 3, 17% with ε 3/ε 4, and 1% with ε 4/ε 4). (
  • Risk factors were age, observation interval, sex (men), and APOE ε 2/ε 2 and ε 2/ε 3 genotypes. (
  • Only 19 of the 88 patients (22%) who developed Alzheimer disease, however, had APOE ε 4/ε 4 ( n = 2) or ε 3/ε 4 ( n = 17) genotypes. (
  • Sex and APOE ε 2/ε 2 or ε 2/ε 3 genotype were not associated with Alzheimer disease. (
  • APOE = apolipoprotein E. (
  • Apolipoprotein E (apoE) is a secretory protein that plays a major role in cholesterol homeostasis in the plasma ( Weisgraber, 1994 ). (
  • Comparison of the APOE allele (E * 2, E * 3, and E * 4) frequencies estimated in this study with those reported for several other population samples showed that there are marked differences between the Dutch population and the populations of Japan, New Zealand, Finland, and the United States. (
  • To test this hypothesis, we investigated the effect of repeated systemic inoculations with Porphyromonas gingivalis ( Pg ), a putative periodontal pathogen, on the progression of atherosclerosis in heterozygous apolipoprotein E-deficient (ApoE +/− ) mice. (
  • However, O 2 − production was significantly reduced in GCH-Tg/ ApoE-KO mice measured both in aortic sections using oxidative confocal microtopography and in whole aorta by lucigenin enhanced chemiluminescence. (
  • We examined regulatory roles of angiotensin-converting enzyme 2 (ACE2) in the apolipoprotein E (ApoE) knockout (KO) kidneys. (
  • Genetic ACE2 deletion resulted in modest elevations in systolic blood pressure levels and Ang II type 1 receptor expression and reduced nephrin expression in kidneys of the ApoE/ACE2 DKO mice with a decrease in renal Ang-(1-7) levels. (
  • Renal dysfunction and ultrastructure injury were aggravated in the ApoE/ACE2 DKO mice and Ang II-infused ApoEKO mice with increased plasma levels of creatinine, blood urea nitrogen and enhanced levels of Ang II in plasma and kidneys. (
  • Apolipoprotein E (APOE4) is the most important known genetic risk for AD and is prevalent in 20-25% of Canadians, but at present, knowing an individual's ApoE genotype does not help the diagnosis, treatment or prevention of AD. (
  • Specific Aim : In the brain, apolipoprotein E(ApoE) is secreted from astrocytes and microglias, and plays important roles in lipid transportation. (
  • To address this question, in this study, we examine for the first time the renoprotective actions of alagebrium in diabetic RAGE apolipoprotein E ( apoE ) double-knockout (KO) mice, with a particular emphasis on glomerular fibrosis and inflammation, comparing its effects with those of the ACE inhibitor, quinapril. (
  • Apolipoprotein E (ApoE) is a protein component of plasma lipoproteins that mediates the binding, internalization and catabolism of lipoprotein particles. (
  • Three major isoforms of ApoE have been described in human (E2, E3 and E4) which differ by only one or two amino acids. (
  • The apolipoprotein E (apoE) genotype is a major genetic determinant of LDL size. (
  • 66 apoE 3/3, 8 apoE 4/3, 10 apoE 3/2) were subjected to 3 dietary periods, each lasting 4 wk. (
  • 0.04) in subjects with the apoE 4/3 genotype compared with those with apoE 3/3 and apoE 3/2 in the basal state. (
  • The apolipoprotein (APOE) epsilon4 allele is a genetic risk factor for the development of Alzheimer's disease (AD). (
  • VL - 483 IS - 1 N2 - The apolipoprotein (APOE) epsilon4 allele is a genetic risk factor for the development of Alzheimer's disease (AD). (
  • The hyperlipideamic apolipoprotein e-knockout (ApoE-/-) mouse is a well-established animal model system for studying the mechanisms of the atherosclerotic process. (
  • Hypertension was induced in hyperlipidemic apolipoprotein-e-knockout (ApoE-/-) mice by application of angiotensin-II and the mice were exposed to mainstream smoke from the reference cigarette 2R4F (University of Kentucky) for 30 days. (
  • AAA formation was seen only in angiotensin-ii treated ApoE-/--mice. (
  • To determine the ability of apolipoprotein E ( APOE ) genotypes to predict days of unconsciousness and a suboptimal functional outcome in traumatic brain injury (TBI) survivors. (
  • The gene that is responsible for the production of apolipoprotein E (apoE) is an attractive candidate for predicting outcome after TBI. (
  • apoE is one of the best-characterized apolipoproteins with respect to structure and function. (
  • 2 - 4 In the nervous system apoE is engaged in the redistribution of cholesterol from cells during membrane synthesis, and neuritic extension growth and repair. (
  • Objective: The angiotensin II (AngII)-infused apolipoprotein E-deficient (ApoE−/−) mouse model is widely used to study atherosclerosis and abdominal aortic aneurysm. (
  • We have shown previously that apolipoprotein A (apoA)-I-containing high-density lipoprotein (HDL) particles are formed by the conjugation of lipid-free apoA-I with lipids derived from other lipoprotein fractions in a process dependent on non-esterified fatty acids, generated by the lipolysis of very-low-density lipoprotein (VLDL) or provided exogenously. (
  • Apolipoprotein A-II (apoA-II), the second major high-density lipoprotein (HDL) apolipoprotein, has been linked to familial combined hyperlipidemia. (
  • Duchateau PN, Pullinger CR, Orellana RE, Kunitake ST, Naya-Vigne J, O'Connor PM, Malloy MJ and Kane JP: Apolipoprotein L, a new human high density lipoprotein apolipoprotein expressed by the pancreas. (
  • The Ratio of High-Density Lipoprotein Cholesterol to Apolipoprotein A-I Predicts Myocardial Injury Following Elective Percutaneous Coronary Intervention. (
  • Prior studies have found inverse associations between high-density lipoprotein cholesterol (HDL-C) or apolipoprotein A-I levels and cardiovascular disease (CVD). (
  • OBJECTIVE To examine the association of renal function in diabetic patients with apolipoprotein (apo) E polymorphism. (
  • Apolipoprotein H (beta-2-glycoprotein I) polymorphism in Asians. (
  • All the studies that have investigated the relation between apolipoprotein E polymorphism and Alzheimer's disease have included highly selected patients and corresponding controls. (
  • By isoelectric focusing of delipidated sera followed by immunoblotting we studied the apolipoprotein (apo) E polymorphism in 2018 randomly selected 35-years-old males from three different areas in the Netherlands. (
  • Boerwinkle E, Utermann G (1988) Simultaneous effects of the apolipoprotein E polymorphism on apolipoprotein E, apolipoprotein B, and cholesterol metabolism. (
  • The role of the apolipoprotein E polymorphism in determining levels, variability, and covariability of cholesterol, beta-lipoprotein, and triglycerides in a sample of unrelated individuals. (
  • Ehnholm C, Lukka M, Kuusi T, Nikkilä E, Utermann G (1986) Apolipoprotein E polymorphism in the Finnish population: gene frequencies and relation to lipoprotein concentrations. (
  • El-Lebedy D, Raslan HM, Mohammed AM. Apolipoprotein E gene polymorphism and risk of type 2 diabetes and cardiovascular disease. (
  • Structures of apolipoprotein A-II and a lipid-surrogate complex provide insights into apolipoprotein-lipid interactions. (
  • 2-Aminopurine inhibits lipid accumulation induced by apolipoprotein E-deficient lipoprotein in macrophages: potential role of eukaryotic initiation factor-2 α phosphorylation in foam cell formation," Journal of Pharmacology and Experimental Therapeutics , vol. 326, no. 2, pp. 395-405, 2008. (
  • When lipid-free apoA-II was incubated with either VLDLs and lipoprotein lipase or LDLs and sodium oleate, a significant proportion of the apoA-II was recovered in the HDL density fraction. (
  • When both lipid-free apoA-I and lipid-free apoA-II were incubated with LDL and sodium oleate, both apolipoproteins were recovered in HDLs that contained phospholipids and unesterified cholesterol as their main lipids. (
  • Patients who have ESRD and undergo hemodialysis (HD) are at increased risk for coronary artery disease (CAD) ( 1,2 ⇓ ), which is due at least in part to lipid abnormalities, typically called uremic dyslipidemia ( 3 ). (
  • Therefore, a role for these apolipoproteins in fatty acid recruitment from triglycerides for surfactant lipid synthesis can be postulated. (
  • Eto M, Watanabe K, Ishii K (1986b) Reciprocal effects of apolipoprotein E alleles (ɛ2 and ɛ4) on plasma lipid levels in normolipidemic subjects. (
  • This comprehensive book provides not only the stages in the development of this unique and specialized field but also updates on the current state of research and development of apolipoprotein mimetics as therapeutic modalities for various lipid-mediated disorders. (
  • Apolipoprotein measurements may provide more detail about your risk for heart disease, but the added value of this test beyond a lipid panel is unknown. (
  • In this study, we examined the association between soy isoflavones and lipid profiles, apolipoprotein levels in patients with type 2 diabetes in China. (
  • Plasma lipid and apolipoprotein levels in children hereditarily predisposed to coronary heart disease. (
  • Lipid-free human apolipoprotein C-II (apoC-II) forms characteristic amyloid fibrils and is one of several apolipoproteins that accumulate in amyloid deposits located within atherosclerotic plaques. (
  • Apolipoprotein C-II and lipoprotein lipase show a temporal and geographic correlation with surfactant lipid synthesis in preparation for birth. (
  • A noticeable increase in surfactant lipid content was measured before the end of gestation day 18, which correlates temporally with the presence of apoC-II in secretory granules in distal epithelium with no or small lumina but not with large lumina. (
  • This study demonstrates that apoC-II and LPL mRNAs correlate temporally and geographically with surfactant lipid synthesis in preparation for birth and suggests that fatty acid recruitment from the circulation by apoC-II-activated LPL is regionally modulated by apoC-II secretion. (
  • Weinberg RB, Spector MS (1985) Structural properties and lipid binding of human apolipoprotein AIV. (
  • T (rs2075291) in apolipoprotein A5 gene to determination of triglycerides levels in CAD patients receiving, atorvastatin, lipid lowering drug. (
  • HealthDay)-Apolipoprotein (apo) CIII and apoCIII-to-apoA1 ratio are correlated with incident type 2 diabetes (T2D), according to a study published online Dec. 28 in Diabetes Care . (
  • Here, our aim was to examine whether VLDL and apolipoprotein (apo) CIII induce endoplasmic reticulum (ER) stress, inflammation and insulin resistance in skeletal muscle. (
  • Hiukka A, Fruchart-Najib J, Leinonen E, Hilden H, Fruchart JC, Taskinen MR (2005) Alterations of lipids and apolipoprotein CIII in very low density lipoprotein subspecies in type 2 diabetes. (
  • Apolipoprotein CIII (ApoCIII) is a 79 amino acids long glycoprotein that is synthesized predominantly in the liver and to a lesser degree in the intestine. (
  • LDL-cholesterol (LDL- C), apolipoproteins (apo) B, CIII, and E, and by decreased levels of HDL-cholesterol (HDL-C), apoA-I, and lecithin:cholesterol acyltransferase (LCAT) activity. (
  • To determine the association between the e4 allele of apolipoprotein E and Alzheimer's disease in a randomly selected population sample. (
  • The prevalence of Alzheimer's disease was 2.9% in subjects with no e4 alleles, 7.6% in subjects with one e4 allele, and 21.4% in subjects with two e4 alleles of apolipoprotein E. (
  • Allele e4 of apolipoprotein is associated with Alzheimer's disease in a dose-response fashion in a randomly selected elderly population. (
  • The first evidence that e4 allele of apolipoprotein E could be associated with Alzheimer's disease was published by Pericak-Vance et al. (
  • Measurements of plasma cholesterol and apo B and E concentrations showed that the E * 4 allele is associated with elevated plasma cholesterol and apo B levels and with decreased apo E concentrations, whereas the opposite is true for the E * 2 allele. (
  • Eto M, Watanabe K, Ishii K (1986a) A racial difference in apolipoprotein E allele frequencies between the Japanese and Caucasian populations. (
  • The apolipoprotein e4 allele on chromosome 19 is an important risk factor for cognitive decline. (
  • We observed a significantly increased risk of cognitive decline associated with a lower level of education in subjects without an apolipoprotein e4 allele. (
  • The HTG patients showed similar allele frequencies of the APOA5, APOC3 and LPL polymorphisms, whereas the NDCP showed similar allele frequencies as the normolipidemic APOE2/2. (
  • This positive effect was more prominent among individuals entering the trial with, (i) higher MMSE scores, (ii) cholesterol levels above 200 mg/dl or (iii) if they harbored an apolipoprotein-E-4 allele compared with participants not responding to atorvastatin treatment. (
  • Individuals in the placebo group tended to experience more pronounced deterioration if their cholesterol levels exceeded 200 mg/dl or they harbored an apolipoprotein-E-4 allele. (
  • Hepatic cell-specific expression of the human apolipoprotein B (apoB) gene is controlled by at least four cis-acting elements located between positions -128 and +122 [Chuang, S. S., & Das, H. K. (1996) Biochem. (
  • ApoB gene regulatory factor-2 (BRF-2) interacts with the sequence (-104 to -85). (
  • These results suggest that BRF-2 and XAP-1 are structurally and immunologically highly related trans-activators of the apoB gene. (
  • AIMS: To explore the association between carotid intima-media thickness (IMT) and the apolipoprotein B (apoB)/apolipoprotein A-I (apoA-I) ratio compared with conventional lipids in middle-aged patients with Type 2 diabetes. (
  • CONCLUSIONS: We conclude that there was a significant association between the apoB/apoA-I ratio and IMT in middle-aged patients with Type 2 diabetes. (
  • The analyst should use the special sampling weights in this file to analyze Apolipoprotein B (ApoB). (
  • Apolipoprotein B (ApoB) consists of a single polypeptide chain with a molecular weight of 549 kDa and is mostly synthesised in the liver. (
  • We determined whether two host defense factors that inhibit AIP1-induced agrI signaling, Nox2 and apolipoprotein B (apoB), also contribute to innate control of AIP3-induced agrIII signaling. (
  • The apolipoprotein A-V genotype and plasma apolipoprotein A-V and triglyceride levels: prospective risk of type 2 diabetes. (
  • To determine if benefit on ADAS-cog performance produced by atorvastatin is influenced by severity of cognitive impairment, circulating cholesterol levels, or apolipoprotein E genotype. (
  • The Apolipoprotein E genotype was established for each participant. (
  • Atorvastatin therapy may be of benefit in the treatment of mild-to-moderately affected AD patients, but the level of benefit produced may be predicated on earlier treatment, an individual's apolipoprotein E genotype or whether the patient exhibits elevated cholesterol levels. (
  • Whether this observation is consistent across low-density lipoprotein cholesterol (LDL-C) levels or total atherogenic particle burden (apolipoprotein B100) is less well-studied, particularly in women. (
  • To determine the association between HDL-C or apolipoprotein A-I level and CVD across a range of LDL-C and apolipoprotein B100 values. (
  • Participants were at low risk for CVD, the number of events in the lowest apolipoprotein B100 stratum was small, only a single baseline measurement was obtained, and residual confounding may have occurred. (
  • Apo-B exists in human plasma in two isoforms, Apo-B48 and Apo-B100. (
  • In the present study, we show that this process is also able to generate HDL particles containing apoA-II (A-II HDL) and both apoA-I and apoA-II (A-I/A-II HDL). (
  • ApoA-I and apoA-II were both present in the larger HDLs, whereas only apoA-I was present in the smaller particles. (
  • Immunoaffinity chromatography on an anti-(apoA-I)-Sepharose column revealed that 10-20% of the apoA-II resided in particles that also contained apoA-I. The majority of the A-I/A-II HDL were present in a population of pre-β2 particles of 10.8 nm diameter. (
  • These results in vitro illustrate a potential mechanism for the formation of HDLs containing both apoA-I and apoA-II. (
  • Human apoA-II transgenic mice constitute an animal model for this proatherogenic disease. (
  • When challenged with an atherogenic diet, antigens related to low-density lipoprotein (LDL) oxidation were markedly increased in the aorta of 11.1 transgenic mice (high human apoA-II expressor). (
  • In contrast, incubation of isolated human apoA-II with control mouse plasma at 37°C decreased PON1 activity and displaced the enzyme from HDL. (
  • Further, the displacement of PON1 by apoA-II could explain in part why PON1 is mostly found in HDL particles with apoA-I and without apoA-II, as well as the poor antiatherogenic properties of apoA-II-rich HDL. (
  • HDLs are classified according to their content of major apolipoproteins: apolipoprotein A-I (apoA-I) and apoA-II. (
  • 1 In contrast, the role of apoA-II is less understood, 2,3 and overexpression of mouse 4 and human apoA-II has generally been found to be proatherogenic. (
  • 5-8 One mechanism by which the apoA-II expression may promote atherogenesis is altered reverse cholesterol transport. (
  • 11 Although antioxidant properties have been ascribed to apoA-I and apoA-II, 12 it is currently believed that an important part of HDL antioxidant properties is related to their associated enzymes. (
  • Low levels of HDL cholesterol and its major apoprotein constituents apoA-I and apoA-II are common in patients who have ESRD and are undergoing hemodialysis (HD), but the metabolic basis for the low HDL is poorly understood. (
  • HDL cholesterol, apoA-I, and apoA-II levels were markedly decreased in the ESRD-HD patients by 39, 30, and 44%, respectively, in comparison with the control subjects. (
  • Conversely, the apoA-II production rate significantly decreased by 31% to 1.50 ± 0.61 mg/kg per d in the ESRD-HD patients in comparison with control subjects of 2.17 ± 0.40 mg/kg per d ( P = 0.047) with apoA-II fractional catabolic rate unchanged. (
  • These results revealed that the decreased levels of apoA-I are due solely to the increased rate of catabolism, whereas the reduced apoA-II levels are due primarily to the decreased rate of production in ESRD-HD patients. (
  • This differential regulation of apoA-I and apoA-II further supports the concept that apoA-I and apoA-II have distinct metabolic pathways. (
  • Three different positive signals with the anti-apoA-II antibody were found: one transient signal in the nucleus of a portion of mesenchymal cells, a second at lower levels throughout the mesenchyme, and another in capillaries with a specific increase from gestation day 17.5/18.5. (
  • Choose from our Apolipoprotein A-II/ApoA2 polyclonal antibodies and browse our Apolipoprotein A-II/ApoA2 monoclonal antibody catalog. (
  • Apolipoprotein A-II antibody LS-C505484 is an AP-conjugated goat polyclonal antibody to human Apolipoprotein A-II. (
  • Immunohistochemistry (below the yellow line) (G-O) was performed using an anti-apoC-II polyclonal antibody (G to I, K to M, O) or goat IgG as negative control (J, N). Positive signals (red) were found in secretory granule-like structures in distal epithelial cells on GD 19.5 (H) and PN0 (G) but not in later timepoints. (
  • METHODS: We analysed data from 247 patients with Type 2 diabetes, aged 55-66 years, in the Cardiovascular Risk factors in Patients with Diabetes-a Prospective study in Primary care (CARDIPP-1) study. (
  • In order to test whether hyperlipidaemia and glycaemic control can be improved among diabetes patients by dietary supplementation with purified omega-3 fatty acids, we carried out a double-blind, placebo-controlled trial on 50 type 2 diabetes patients randomized to 2 g/day purified omega-3 fatty acids or placebo for 10 weeks. (
  • The prevalence of type 2 diabetes has increased greatly in the past few years, and an even greater increase is foreseen in the next few years [1]. (
  • C and S19W genotypes were determined in 2,490 men, of whom 145 subsequently developed type 2 diabetes. (
  • 0.002) and were not different in men who subsequently developed type 2 diabetes compared with healthy men (p=0.7). (
  • C or S19W was found on type 2 diabetes risk.Conclusions/interpretation In contrast to animal studies, in man, plasma APOA5 positively correlates with plasma triglyceride levels. (
  • In prospective analysis, with the caveat that numbers were small, APOA5 genotypes do not appear to have an impact on risk of development of type 2 diabetes. (
  • The study shows that approximately two ounces of nuts a day, as a replacement for carbohydrate foods, can improve glycemic control and blood lipids in those with type 2 diabetes. (
  • The study population was composed of 120 cases (80 women with type 2 diabetes and 40 healthy women). (
  • Soy product and isoflavone intakes are associated with a lower risk of type 2 diabetes in overweight Japanese women. (
  • The results demonstrate the important role of both intra- and inter-subunit charge interactions in stabilizing apoC-II amyloid fibrils, a process that may be a key factor in determining the general ability of proteins to form amyloid fibrils. (
  • Using the models of two long anti-atherogenic and anti-inflammatory proteins (apolipoprotein A-I and apolipoprotein E with 243 and 299 amino acids, respectively) short mimetic peptides of 18 to 28 amino acid residues in length, which can be produced either synthetically or genetically in edible fruits and vegetables, have been shown to exert profound biological effects in a large number of animal models of diseases. (
  • New vessels grow into the vitreous cavity, which consists of various extracellular matrix (ECM) proteins, resulting in traction retinal detachment and vitreous hemorrhage ( 2 ). (
  • Apolipoprotein J Antibody functions as a secreted chaperone that prevents aggregation of nonnative proteins. (
  • Apolipoprotein J does not require ATP or refold proteins by itself. (
  • This product has been prepared by immunoaffinity chromatography using immobilized antigens followed by extensive cross-adsorption against other apoLipoproteins and human serum proteins to remove any unwanted specificities. (
  • Non-specific cross reaction of anti-apoLipoprotein antibodies with other human serum proteins is negligible. (
  • Apolipoproteins are proteins on the surface of the lipoprotein complex that bind to specific enzymes or transport proteins on the cell membranes. (
  • Each Apolipoprotein A-II/ApoA2 Antibody is fully covered by our Guarantee+, to give you complete peace of mind and the support when you need it. (
  • Finally, incubation of myotubes with a neutralising antibody against Toll-like receptor 2 abolished the effects of apoCIII on ER stress, inflammation and insulin resistance, indicating that the effects of apoCIII were mediated by this receptor. (
  • Anti-Apolipoprotein J Antibody is useful for researchers interested in the immune system, Ubiquitin pathways, and cardiovascular research. (
  • This antibody reacts with human apoLipoprotein J and has negligible cross-reactivity with Type A-I, A-II, B, C-I, C-II, C-III and E apoLipoproteins. (
  • No. R1029P Apolipoprotein AI antibody staining of Paraffin-Embedded Human Liver. (
  • No. R1031P Apolipoprotein AII antibody staining of Paraffin-Embedded Human Adrenal at 5 µg/ml. (
  • No. AP16668PU-N APOA4 antibody staining of Paraffin Embedded Human Intestine at 2 µg/ml. (
  • No. AP16949PU-N Apolipoprotein CI antibody Staining of Paraffin Embedded Human Liver at 3.8 µg/ml. (
  • Single doses of peptides Ac-hE18A-NH(2) and mR18L were administered retro-orbitally to LDL-R null mice on Western diet and plasma cholesterol was measured at 10 min, 4 h, and 24 h post administration. (
  • Peptide mR18L and not Ac-hE18A-NH(2) reduced plasma cholesterol levels significantly at 4 h post administration. (
  • Plasma apolipoprotein E phenotypes modulate lipoprotein concentrations, particularly that of low density lipoprotein cholesterol. (
  • Hyperlipoproteinemia type II is further classified into types IIa and IIb, depending mainly on whether elevation in the triglyceride level occurs in addition to LDL cholesterol. (
  • Laboratory findings for these individuals are significant for total serum cholesterol levels two to three times greater than normal, as well as increased LDL cholesterol, but their triglycerides and VLDL values fall in the normal ranges. (
  • NFκB regulates plasma apolipoprotein A-I and HDL-cholesterol through inhibition of PPARα'Journal of Biological Chemistry. (
  • KFκB regulates plasma apolipoprotein A-I and HDL-cholesterol through inhibition of PPARα'Journal of Biological Chemistry. (
  • Apolipoprotein CI (ApoCI) functions as a cofactor for LCAT (lecithin-cholesterol acyltransferase), the enzyme responsible for most plasma cholesterol esterification. (
  • Chen CH, Albers JJ (1985) Activation of lecithin:cholesterol acyltransferase by apolipoproteins E-2, E-3, and AIV isolated from human plasma. (
  • In the present study we further investigated regulation of apoM expression in Caco-2 cells stimulated by a liver X receptor (LXR) agonist, TO901317. (
  • The amino acid sequences of two tryptic peptides derived from HPLC-purified heavier BRF-2 isoform were determined to be YLAIAPPIIK and ALYYLQIHPQELR. (
  • Anti-peptide antisera raised against two synthetic peptides of XAP-1 recognized a approximately 120-kDa polypeptide band in both BRF-2 isoforms in a western blot analysis. (
  • Both peptides reduced total plaque macrophage load compared to the saline treated animals, with peptide Ac-hE18A-NH(2) having a greater reduction. (
  • Dr. Goldberg is President and Co-Founder of LipimetiX Development, LLC, a biotechnology company developing apolipoprotein E mimetic peptides licensed from the University of Alabama at Birmingham Research Foundation. (
  • The active peptide of apo C - II corresponds to residues 44 - 79 and has been identified to reverse the symptoms of genetic apo C - II deficiency. (
  • The report of recognizable cognitive changes in nuns half a century before the development of frank Alzheimer disease ( 2 ) could conceivably be used as a pretext to justify genetic screening for jobs that require intellectual capacity. (
  • Therefore, it has been attempted to identify the specific genetic determinants of plasma TG levels, and a novel member of the apolipoprotein family, apolipoprotein A5 (APOA5), was identified by the comparative sequencing of the APOA1/C3/A4 gene cluster region [ 3 ]. (
  • Genetic evidence indicates that apolipoprotein E4 (apoE4) is a risk factor for the development of Alzheimer's disease. (
  • Genetic factors contributing to the expression of type III HLP were investigated in 113 hyper- and 52 normolipidemic E2/2 subjects, by testing for polymorphisms in APOC3, APOA5, HL (hepatic lipase) and LPL (lipoprotein lipase) genes. (
  • In this paper we report the isolation of two isoforms of BRF-2 by further purification using high-performance liquid chromatography. (
  • Your search returned 1 apolipoprotein B mRNA editing enzyme catalytic subunit 2 ELISA ELISA Kit across 1 supplier. (
  • Histomorphometry of plaque cross-sectional area in the proximal aortas, en face measurement of plaque area over the aortic trees, Pg 16S ribosomal DNA amplification with polymerase chain reaction, ELISA for systemic proinflammatory mediators, and immunolocalization of macrophages in the proximal aorta were performed. (
  • Anti-apolipoprotein antibodies have been used for indirect trapping ELISA for quantitation of antigen in serum using a standard curve, for immunoprecipitation and for western blotting for highly sensitive qualitative analysis. (
  • Typically less than 1% cross reactivity against other types of apoLipoprotein was detected by ELISA against purified standards. (
  • 27 Apolipoprotein C-II (APOC2) Kits ELISA de 9 fabricants sont disponibles sur (
  • RF 1-2* Evidence is accumulating that apolipoprotein E is important in late onset Alzheimer's disease. (
  • Verghese, P. B., Castellano, J. M. & Holtzman, D. M. Apolipoprotein E in Alzheimer's disease and other neurological disorders. (
  • TY - JOUR T1 - Apolipoprotein epsilon4 and neuropsychological performance in Alzheimer's disease and vascular dementia. (
  • Our Apolipoprotein A-II/ApoA2 Antibodies can be used in a variety of model species: Human. (
  • Conformational rearrangement of apoC-II at lipoprotein surfaces promotes interaction with LPL (show LCP1 Antibodies ). (
  • In an immunochemical reaction, Apolipoprotein B in the human serum sample form immune complexes with specific antibodies. (
  • In autoimmune disease, anti-apolipoprotein H (AAHA) antibodies, also called anti-β2 glycoprotein I antibodies, comprise a subset of anti-cardiolipin antibodies and lupus anticoagulant. (
  • Specific cross reaction of anti-apoLipoprotein antibodies with antigens from other species has not been determined. (
  • RDN decreased systolic blood pressure in apolipoprotein E-deficient mice. (
  • RDN did not affect the size of aortic aneurysms formed or the incidence of aortic rupture in mice receiving angiotensin II. (
  • The higher MMP-2 expression could be the results of the greater amount of atheroma in the RDN mice. (
  • Skeletal muscle from transgenic mice overexpressing apoCIII showed increased levels of some ER stress and inflammatory markers and increased phosphorylated ERK1/2 levels, whereas PGC-1α levels were reduced, confirming apoCIII effects in vivo. (
  • The Ang II-mediated reductions of renal ACE2 and nephrin levels in ApoEKO mice were remarkably rescued by rhACE2 supplementation, along with augmentation of renal Ang-(1-7) levels. (
  • More importantly, rhACE2 treatment significantly reversed Ang II-induced renal inflammation, superoxide generation, kidney dysfunction and adverse renal injury in ApoEKO mice with suppression of the NOX4 and TNF-alpha-TNFRSF1A signaling. (
  • Expression of matrix metalloproteinases-(MMP)-2, -3, -8, -9, and -12 in AAA was enhanced in smoke-exposed angiotensin-II treated hyperlipemic mice. (
  • Zymographic activity analysis revealed that the activity of MMP-9 and MMP-2 was highest in the mice exposed to all three risk factors. (
  • Here, we studied the role of LPL and two potent modifiers, the LPL inhibitor apoC-III and the LPL activator apoA-V, in APOE2-knockin (APOE2) mice. (
  • Structure of a biologically active fragment of human serum apolipoprotein C-II in the presence of sodium dodecyl sulfate and dodecylphosphocholine. (
  • Both an excess and deficiency of apo C - II is associated with hypertriglyceridemia and reduced LPL activity. (
  • Whilst extremely rare, a deficiency in apo C-II results in excess fasting hypertriglyceridemia and chylomicronemia. (
  • Biologically and clinically, apo C - II deficiency closely mimics LPL deficiency. (
  • Synonyms for apo C-II deficiency include: C - II an apolipoproteinemia and hyperlipoproteinemia type Ib 5 . (
  • Hoffmann MM, März W. Apo C-II Deficiency. (
  • Large deletion in APOC2 caused by Alu-Alu homologous recombination is associated with with apolipoprotein C-II deficiency. (
  • Familial apo-A-II deficiency may result from a splice-junction alteration which blocks splicing of intron 3 from the primary transcript and result the formation of a non-functional mRNA. (
  • Type I hyperlipoproteinemia exists in several forms: Lipoprotein lipase deficiency (type Ia), due to a deficiency of lipoprotein lipase (LPL) or altered apolipoprotein C2, resulting in elevated chylomicrons, the particles that transfer fatty acids from the digestive tract to the liver Familial apoprotein CII deficiency (type Ib), a condition caused by a lack of lipoprotein lipase activator. (
  • ApoCIII mimicked the effects of VLDL and its effects were also blocked by ERK1/2 inhibition, suggesting that this apolipoprotein was responsible for the effects of VLDL. (
  • As angiotensin II infusion also induces aortic aneurysm we also assessed the effect of RDN on aortic aneurysm severity. (
  • Angiotensin (Ang) II plays a pivotal role in perpetuating glomerular injury in kidney via the modulation of nephrin signaling, the integrity of which is crucial for the glomerular filtration barrier [ 12 ]. (
  • Recently, the sequencing of human genomic DNA has led to the discovery of Apolipoprotein A5 (APOA5) gene which belongs to a regulatory gene family including APOA1, APOC3 and APOA4 [ 5 ].This gene is located on chromosome 11q23 in about 30 kb downstream of APOA4, and contains four exons. (
  • J. Lewerenz and P. Maher, "Basal levels of eIF2 α phosphorylation determine cellular antioxidant status by regulating ATF4 and xCT expression," Journal of Biological Chemistry , vol. 284, no. 2, pp. 1106-1115, 2009. (
  • RDN significantly increased the aortic mRNA expression of matrix metalloproteinase-2 (MMP-2). (
  • Expression of apolipoprotein A-I (apoA-I), A-II, and H was previously observed at 16 to 50-fold higher levels in the fetal than the adult mouse lung. (
  • Start Forskningsoutput TO901317 regulating apolipoprotein M expression mediates via. (
  • Conclusion: The present study demonstrated that LXR agonist TO901317 induced apoM expression in Caco-2 cells might be mediated via the LXR/FXR pathway. (
  • The major sites of apoC-II and LPL gene expression changed over time and were found mainly in the distal epithelium at the end of gestation but not after birth. (
  • Polymorphisms in lipolysis genes associate with the expression and severity of type III HLP in APOE2/2. (
  • 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. (
  • Low-density lipoprotein and apolipoprotein B: clinical use in patients with coronary heart disease. (
  • In multivariable analyses, HDL-C and apolipoprotein A-I levels were inversely associated with CVD and coronary events but not stroke. (
  • Kukita M, Hiwada K, Kokubu T (1984) Serum apolipoprotein A-I, A-II and B levels and their discriminative values in relatives of patients with coronary artery disease. (
  • Tian M, Li R, Shan Z, Wang DW, Jiang J, Cui G. Comparison of Apolipoprotein B/A1 ratio, Framingham risk score and TC/HDL-c for predicting clinical outcomes in patients undergoing percutaneous coronary intervention. (
  • Synchronized inhibition of the phospholipid mediated autoactivation of factor XII in plasma by beta 2-glycoprotein I and anti-beta 2-glycoprotein I". Thromb. (
  • Furthermore, our results showed high binding affinity of rhLK8 to α3β1 integrin and downstream inhibition of activation of FAK, p130 Crk-associated substrate (p130CAS), and c-Jun NH 2 -terminal kinase (JNK). (
  • Apolipoproteins E" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (
  • Only the plasma from the Ac-hE18A-NH(2) group had significantly reduced reactive oxygen species levels at the end of the treatment protocol. (
  • Both mR18L and Ac-hE18A-NH(2) showed reduced atherosclerotic lesion areas. (
  • 1,2 ⇓ Recent studies have suggested associations of atherosclerotic risk with infectious agents, 1-3 ⇓ ⇓ and several pathogens such as Chlamydia pneumoniae , Helicobacter pylori , Cytomegalovirus, herpes simplex virus, Streptococcus sanguis, and Porphyromonas gingivalis have been detected in human atheromas. (
  • 2 ) reported using surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS) to identify three biomarkers that simultaneously improved the detection of early-stage ovarian cancer, in particular test specificity. (
  • Targeted mass spectrometric immunoassays toward apolipoproteins A-I, A-II, and C-III were applied on large cross-sectional and longitudinal clinical cohorts. (
  • Baseline lipids were measured directly, and apolipoproteins were measured with immunoassays. (
  • 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. (
  • 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. (
  • The determination of the circulating levels of apolipoproteins has become common practice in clinical laboratories, in view of the apparent correlation between levels of specific apolipoproteins and increased or decreased cardiovascular risk [1, 2]. (