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 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.
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.
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 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.
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 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).
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.
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.
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.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
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 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.
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 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.
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 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)
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.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
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)
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
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.
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 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.
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.
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.
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.
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 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 family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).
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.
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.
A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Conditions with excess LIPIDS in the blood.
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.
Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
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.
The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.
The main trunk of the systemic arteries.
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.
A diet that contributes to the development and acceleration of ATHEROGENESIS.
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.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.
Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.
Cholesterol 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.
An individual having different alleles at one or more loci regarding a specific character.
An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
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.
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.
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).
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.)
A condition of elevated levels of TRIGLYCERIDES in the blood.
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.
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.
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 latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
An individual in which both alleles at a given locus are identical.
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.
Pathological processes involving any part of the AORTA.
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.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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.
Cholesterol present in food, especially in animal products.
Lipid-laden macrophages originating from monocytes or from smooth muscle cells.
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.
A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.
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 .
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
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.
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)
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
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.
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.
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.
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.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
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.
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.
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.
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.
The rate dynamics in chemical or physical systems.
Disturbances in mental processes related to learning, thinking, reasoning, and judgment.
Lesions formed within the walls of ARTERIES.
Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.
An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.
Accumulations of extracellularly deposited AMYLOID FIBRILS within tissues.
The age, developmental stage, or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual.
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.
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.
Abnormal structures located in various parts of the brain and composed of dense arrays of paired helical filaments (neurofilaments and microtubules). These double helical stacks of transverse subunits are twisted into left-handed ribbon-like filaments that likely incorporate the following proteins: (1) the intermediate filaments: medium- and high-molecular-weight neurofilaments; (2) the microtubule-associated proteins map-2 and tau; (3) actin; and (4) UBIQUITINS. As one of the hallmarks of ALZHEIMER DISEASE, the neurofibrillary tangles eventually occupy the whole of the cytoplasm in certain classes of cell in the neocortex, hippocampus, brain stem, and diencephalon. The number of these tangles, as seen in post mortem histology, correlates with the degree of dementia during life. Some studies suggest that tangle antigens leak into the systemic circulation both in the course of normal aging and in cases of Alzheimer disease.
A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.
A single-pass type I membrane protein. It is cleaved by AMYLOID PRECURSOR PROTEIN SECRETASES to produce peptides of varying amino acid lengths. A 39-42 amino acid peptide, AMYLOID BETA-PEPTIDES is a principal component of the extracellular amyloid in SENILE PLAQUES.
Established cell cultures that have the potential to propagate indefinitely.
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.
Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
Elements of limited time intervals, contributing to particular results or situations.
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).
Relating to the size of solids.
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)
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.
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 dilatation of the aortic wall behind each of the cusps of the aortic valve.
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.
Genotypic differences observed among individuals in a population.
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.
An imprecise term referring to dementia associated with CEREBROVASCULAR DISORDERS, including CEREBRAL INFARCTION (single or multiple), and conditions associated with chronic BRAIN ISCHEMIA. Diffuse, cortical, and subcortical subtypes have been described. (From Gerontol Geriatr 1998 Feb;31(1):36-44)
Proteins prepared by recombinant DNA technology.
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 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.
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.
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Transport proteins that carry specific substances in the blood or across cell membranes.
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.
Substances used to lower plasma CHOLESTEROL levels.
(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.
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.
A mercaptoethylamine compound that is endogenously derived from the COENZYME A degradative pathway. The fact that cysteamine is readily transported into LYSOSOMES where it reacts with CYSTINE to form cysteine-cysteamine disulfide and CYSTEINE has led to its use in CYSTINE DEPLETING AGENTS for the treatment of CYSTINOSIS.
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.
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.
An enzyme of the isomerase class that catalyzes the eliminative cleavage of polysaccharides containing 1,4-linked D-glucuronate or L-iduronate residues and 1,4-alpha-linked 2-sulfoamino-2-deoxy-6-sulfo-D-glucose residues to give oligosaccharides with terminal 4-deoxy-alpha-D-gluc-4-enuronosyl groups at their non-reducing ends. (From Enzyme Nomenclature, 1992) EC 4.2.2.7.
An enzyme which catalyzes the hydrolysis of an aryl-dialkyl phosphate to form dialkyl phosphate and an aryl alcohol. It can hydrolyze a broad spectrum of organophosphate substrates and a number of aromatic carboxylic acid esters. It may also mediate an enzymatic protection of LOW DENSITY LIPOPROTEINS against oxidative modification and the consequent series of events leading to ATHEROMA formation. The enzyme was previously regarded to be identical with Arylesterase (EC 3.1.1.2).
Electrophoresis in which agar or agarose gel is used as the diffusion medium.
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.
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 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.
Microtubule-associated proteins that are mainly expressed in neurons. Tau proteins constitute several isoforms and play an important role in the assembly of tubulin monomers into microtubules and in maintaining the cytoskeleton and axonal transport. Aggregation of specific sets of tau proteins in filamentous inclusions is the common feature of intraneuronal and glial fibrillar lesions (NEUROFIBRILLARY TANGLES; NEUROPIL THREADS) in numerous neurodegenerative disorders (ALZHEIMER DISEASE; TAUOPATHIES).
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.
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.
An enzyme that catalyzes the deamination of cytidine, forming uridine. EC 3.5.4.5.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
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 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.
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.
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.
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.
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.
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.
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)
Mice bearing mutant genes which are phenotypically expressed in the animals.
Colloids formed by the combination of two immiscible liquids such as oil and water. Lipid-in-water emulsions are usually liquid, like milk or lotion. Water-in-lipid emulsions tend to be creams. The formation of emulsions may be aided by amphiphatic molecules that surround one component of the system to form MICELLES.
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).
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.
Identification of genetic carriers for a given trait.
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).
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.
A prodromal phase of cognitive decline that may precede the emergence of ALZHEIMER DISEASE and other dementias. It may include impairment of cognition, such as impairments in language, visuospatial awareness, ATTENTION and MEMORY.
Age as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or the effect of a circumstance. It is used with human or animal concepts but should be differentiated from AGING, a physiological process, and TIME FACTORS which refers only to the passage of time.
Cell surface molecules on cells of the immune system that specifically bind surface molecules or messenger molecules and trigger changes in the behavior of cells. Although these receptors were first identified in the immune system, many have important functions elsewhere.
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.
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.
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 time frame after a meal or FOOD INTAKE.
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.
An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.
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.
Detection of a MUTATION; GENOTYPE; KARYOTYPE; or specific ALLELES associated with genetic traits, heritable diseases, or predisposition to a disease, or that may lead to the disease in descendants. It includes prenatal genetic testing.
Intellectual or mental process whereby an organism obtains knowledge.
Regular course of eating and drinking adopted by a person or animal.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
A condition marked by the development of widespread xanthomas, yellow tumor-like structures filled with lipid deposits. Xanthomas can be found in a variety of tissues including the SKIN; TENDONS; joints of KNEES and ELBOWS. Xanthomatosis is associated with disturbance of LIPID METABOLISM and formation of FOAM CELLS.
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.
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.
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.
Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.
Maleness or femaleness as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or effect of a circumstance. It is used with human or animal concepts but should be differentiated from SEX CHARACTERISTICS, anatomical or physiological manifestations of sex, and from SEX DISTRIBUTION, the number of males and females in given circumstances.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.
Abstaining from all food.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.
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 innermost layer of an artery or vein, made up of one layer of endothelial cells and supported by an internal elastic lamina.
Surface ligands that mediate cell-to-cell adhesion and function in the assembly and interconnection of the vertebrate nervous system. These molecules promote cell adhesion via a homophilic mechanism. These are not to be confused with NEURAL CELL ADHESION MOLECULES, now known to be expressed in a variety of tissues and cell types in addition to nervous tissue.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
Diseases in which there is a familial pattern of AMYLOIDOSIS.
Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
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.
Techniques used to add in exogenous gene sequence such as mutated genes; REPORTER GENES, to study mechanisms of gene expression; or regulatory control sequences, to study effects of temporal changes to GENE EXPRESSION.
Those characteristics that distinguish one SEX from the other. The primary sex characteristics are the OVARIES and TESTES and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
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.
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.
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)

Apo E phenotype and changes in serum lipids in adult patients during growth hormone replacement. (1/187)

OBJECTIVE: To determine whether apo E phenotype influences changes in lipid profiles induced by growth hormone replacement in growth hormone (GH)-deficient adults. DESIGNS: Patients were treated for 6 months with recombinant human GH (hGH), given in a dose of 0.125 U/kg per week for 4 weeks followed by 0.25 U/kg per week thereafter. The effects on serum lipids and the influence of apo E phenotype were examined. METHODS: Thirty patients (aged 35.1+/-11.8 years: mean +/- S.D.) with adult growth hormone deficiency with included in the study. Fasting serum samples were analysed for apo E phenotype total cholesterol, high-density lipoprotein (HDL)-cholesterol, triglycerides, lipoprotein (a) (Lp(a)) and IGF-I. Low-density lipoprotein (LDL)-cholesterol was calculated using the Friedwald formula. RESULTS: Six months of replacement treatment with hGH resulted in a reduction in HDL-cholesterol from 0.90+/-0.10 to 0.68+/-0.08 mmol/l (P<0.01), and a small, non-significant reduction in total cholesterol from 6.14+/-0.40 to 5.99+/-0.35 mmol/l (P = 0.06). There was no significant change in the other lipid parameters. The decrease in HDL-cholesterol concentration was greater in patients carrying the apo E2 allele (0.40+/-0.07 mmol/l, P<0.05) than in patients homozygous for the apo E3 allele (0.23+/-0.04 mmol/l) and patients carrying the apo E4 allele (0.15+/-0.36 mmol/l). Patients with the apo E4 allele had lower baseline cholesterol concentrations than patients lacking the apo E4 allele, and this persisted after treatment with hGH (P<0.05). CONCLUSIONS: Apo E phenotype may be a determining factor in the response of HDL-cholesterol to hGH in GH-deficient adults.  (+info)

Binding of beta-VLDL to heparan sulfate proteoglycans requires lipoprotein lipase, whereas ApoE only modulates binding affinity. (2/187)

The binding of beta-VLDL to heparan sulfate proteoglycans (HSPG) has been reported to be stimulated by both apoE and lipoprotein lipase (LPL). In the present study we investigated the effect of the isoform and the amount of apoE per particle, as well as the role of LPL on the binding of beta-VLDL to HSPG. Therefore, we isolated beta-VLDL from transgenic mice, expressing either APOE*2(Arg158-->Cys) or APOE*3-Leiden (E2-VLDL and E3Leiden-VLDL, respectively), as well as from apoE-deficient mice containing no apoE at all (Enull-VLDL). In the absence of LPL, the binding affinity and maximal binding capacity of all beta-VLDL samples for HSPG-coated microtiter plates was very low. Addition of LPL to this cell-free system resulted in a 12- to 55-fold increase in the binding affinity and a 7- to 15-fold increase in the maximal binding capacity (Bmax). In the presence of LPL, the association constant (Ka) tended to increase in the order Enull-VLDL+info)

Apo E structure determines VLDL clearance and atherosclerosis risk in mice. (3/187)

We have generated mice expressing the human apo E4 isoform in place of the endogenous murine apo E protein and have compared them with mice expressing the human apo E3 isoform. Plasma lipid and apolipoprotein levels in the mice expressing only the apo E4 isoform (4/4) did not differ significantly from those in mice with the apo E3 isoform (3/3) on chow and were equally elevated in response to increased lipid and cholesterol in their diet. However, on all diets tested, the 4/4 mice had approximately twice the amount of cholesterol, apo E, and apo B-48 in their VLDL as did 3/3 mice. The 4/4 VLDL competed with human LDL for binding to the human LDL receptor slightly better than 3/3 VLDL, but the VLDL clearance rate in 4/4 mice was half that in 3/3 mice. On an atherogenic diet, there was a trend toward greater atherosclerotic plaque size in 4/4 mice compared with 3/3 mice. These data, together with our earlier observations in wild-type and human APOE*2-replacement mice, demonstrate a direct and highly significant correlation between VLDL clearance rate and mean atherosclerotic plaque size. Therefore, differences solely in apo E protein structure are sufficient to cause alterations in VLDL residence time and atherosclerosis risk in mice.  (+info)

Apolipoprotein E2/E5 variants in lipoprotein glomerulopathy recurred in transplanted kidney. (4/187)

Lipid abnormalities are associated with various disorders ranging from generalized atherosclerosis to renal diseases, including lipoprotein glomerulopathy that is characterized by glomerular lipoprotein thrombi and causes type III hyperlipoproteinemia, proteinuria, and renal failure. This study examines lipoprotein glomerulopathy, which recurred in a transplanted kidney. Molecular biologic analysis of the patient's apolipoprotein (apo) E gene demonstrated E2/E5 type variants. Immunohistochemical analysis of the diseased kidney demonstrated various lipid peroxidation-specific protein adducts, suggesting a potential role of oxidative stress in this disorder. Recurrence in the transplanted kidney suggested a pathogenic role of extraglomerular humoral component(s) resulting from abnormal lipoprotein metabolism, presumably linked to apo E and other genetic or acquired factor(s). Furthermore, the finding that the patient showed pathologic abnormalities in the transplanted kidney with no clinical signs or symptoms of renal disease indicated that lipoprotein glomerular damage progresses early before any clinical manifestations.  (+info)

A novel apolipoprotein E mutation, E2 (Arg25Cys), in lipoprotein glomerulopathy. (5/187)

BACKGROUND: Lipoprotein glomerulopathy (LPG) is characterized by intraglomerular lipoprotein thrombosis and high plasma concentrations of apolipoprotein (apo) E. An apo E variant, apo E2 (Arg145Pro) Sendai, was recently identified in three patients with LPG. We detected a novel point mutation in the apo E gene in a patient with LPG, and we characterized the mutant apo E. METHODS: The propositus was a 32-year-old male patient on maintenance hemodialysis because of LPG. The mutation was detected by sequencing of genomic DNA from the patient and was confirmed by restriction fragment length polymorphism (RFLP) with Aor51HI. Recombinant apo E2 (Arg25Cys) Kyoto and normal apo E3 were expressed from COS-1 cells. Low-density lipoprotein (LDL) receptor-binding activities of the variants were determined in an in vitro competition assay. RESULTS: The propositus had the apo E phenotype E2/E4, as determined by isoelectric focusing, and the genotype epsilon3/epsilon4, as determined by RFLP with HhaI. Sequence analysis of amplified DNA showed a C to T transition, changing the codon for residue 25 from arginine to cysteine. The proband was a heterozygous carrier for apo E2 (Arg25Cys) Kyoto. A family study showed that the mother was a heterozygous carrier of apo E2 Kyoto and had dysbetalipoproteinemia, but no LPG. The pathophysiological effect of this mutation was investigated in vitro by binding studies of recombinant apo E2 Kyoto to LDL receptors on human fibroblasts. The ability of recombinant apo E2 Kyoto to displace LDL was reduced to 10% compared with recombinant apo E3. CONCLUSIONS: Apo E2 (Arg25Cys) Kyoto is a novel mutation of apo E that is etiologically related to LPG. However, our case indicates that the development of LPG may involve other genetic or environmental factors. Furthermore, our data suggest that arginine-25 of apo E plays an important functional role by influencing the receptor-binding ability of apo E.  (+info)

Cerebral amyloid angiopathy-related hemorrhage. Interaction of APOE epsilon2 with putative clinical risk factors. (6/187)

BACKGROUND AND PURPOSE: Current evidence suggests that the apolipoprotein E (APOE for gene; apoE for protein) epsilon4 allele predisposes to cerebral amyloid angiopathy (CAA) whereas epsilon2 is associated with CAA-related hemorrhage (CAAH). The clinical risk factors for other forms of intracranial hemorrhage are a less-frequent feature of CAAH. In this study we examined potential clinical risk factors in patients with CAAH and assessed these with respect to APOE genotype. METHODS: Thirty-six patients were identified with a pathological diagnosis of CAAH. Clinical notes were reviewed to document age of hemorrhage onset, history of dementia, antiplatelet/anticoagulant medication, hypertension, minor head trauma, or transient neurological events. In a review of reported cases of CAAH, the frequency of these clinical features was also recorded. APOE genotypes were determined with use of polymerase chain reaction techniques. RESULTS: There were 24 women and 12 men; the mean age was 70.3 years. One third (n=12) had been taking antiplatelet medication, and a similar number were demented. Nine patients were hypertensive, and 4 had a history of recent minor head trauma. The relative frequency of each of these clinical features was similar to that in previous reports. Forty-four percent (16 of 36) possessed an epsilon2 allele. Antiplatelet or anticoagulant medication, hypertension, or minor head trauma were significantly more frequent antecedents of CAAH in epsilon2 carriers than in non-epsilon2 carriers (81% versus 35%, P=0.008), antiplatelet/anticoagulant medication in particular (P=0.038). CONCLUSIONS: Our findings suggest that antiplatelet or anticoagulant medication, hypertension, or minor head trauma are most likely to precipitate cerebral hemorrhage in patients with CAA who are also epsilon2 carriers. This may result from isoform-specific effects of apoE on the structure of amyloid-laden blood vessel walls.  (+info)

Independent effects of Apo E phenotype and plasma triglyceride on lipoprotein particle sizes in the fasting and postprandial states. (7/187)

LDL particle sizes and Apo E phenotypes were determined in 212 subjects of whom 51 had angina. LDL diameter was significantly less in subjects with an epsilon2 allele (24.76+/-0.08 vs 24.94+/-0.02 nm, P=0.02), and this was evident for both E2/E3 (24.77+/-0.09 nm) and E2/E4 (24.69+/-0.08 nm) phenotypes. Although there was a negative relation between LDL diameter and plasma triglyceride, the effect of apo E2 was still evident with adjustment for triglyceride. In multiple regression analysis, the significant determinants of LDL diameter were gender (with females having larger particles than males), body mass index, and the presence (or absence) of E2. HDL particle sizes and compositions were determined on fasting samples and, additionally, 5 and 8 hours after a fat-rich meal for 48 coronary heart disease cases and 49 control subjects. Fasting HDL particle sizes were not related to the presence of E2 but were significantly smaller for subjects possessing an epsilon4 allele (8. 09+/-0.08 vs 8.39+/-0.05 nm, P=0.003) and were negatively related to plasma triglyceride. However, the effect of E4 persisted after adjustment for triglyceride. In a multiple regression analysis, the only significant determinant of fasting HDL diameter was the presence (or absence) of E4 with fasting plasma triglyceride just failing to reach significance (P=0.06). There was a postprandial increase in HDL diameter that was less marked in subjects with coronary heart disease. The postprandial increase in HDL diameter was of sufficient magnitude to result in size reclassification of HDL particles. The influence of E4 was also evident at both postprandial time points. Compositional analysis demonstrated that the increase in HDL diameters postprandially could be attributed to triglyceride enrichment, with an accompanying fall in cholesterol ester content. Phospholipid changes postprandially were biphasic with an initial fall followed by a rise in concentration. The increase in triglyceride content was significantly less in those subjects with angina despite an equivalent rise in plasma triglyceride. The present study demonstrates significant, but different, effects of variation in apo E phenotype on the particle sizes of both HDL and LDL. Such effects were still evident with adjustment for differences in plasma triglyceride and suggests that variation in apo E phenotype exerts effects on lipoprotein particle sizes by mechanisms additional to those dependent on change in plasma triglyceride.  (+info)

Pathogenesis of type III hyperlipoproteinemia (dysbetalipoproteinemia). Questions, quandaries, and paradoxes. (8/187)

Type III hyperlipoproteinemia (HLP) is a genetic disorder characterized by accumulation of remnant lipoproteins in the plasma and development of premature atherosclerosis. Although receptor binding-defective forms of apolipoprotein (apo) E are the common denominator in this disorder, a number of apparent paradoxes concerning its pathogenesis still exist. However, studies in transgenic animals are resolving the mechanisms underlying this disorder. PARADOX I: Defective apoE (commonly apoE2) is essential but not sufficient to cause overt type III HLP. In fact, most apoE2 homozygotes are hypolipidemic. Studies in apoE2 transgenic models have demonstrated the impact of other genes or hormones in converting the hypolipidemia to hyperlipidemia. PARADOX II: Among apoE2 homozygotes, men are more susceptible than women to type III HLP. Transgenic studies have shown that estrogen affects both LDL receptor expression and lipolytic processing, explaining the resistance of women to this disorder until after menopause. PARADOX III: ApoE deficiency is associated with hypercholesterolemia, whereas the type III HLP phenotype is characterized by both hypercholesterolemia and hypertriglyceridemia. The hypercholesterolemia is caused by impaired receptor-mediated clearance, whereas the hypertriglyceridemia is caused primarily by impaired lipolytic processing of remnants and increased VLDL production associated with increased levels of apoE. PARADOX IV: ApoE2 is associated with recessive inheritance of this disorder, whereas other defective apoE variants are associated with dominant inheritance. Determinants of the mode of inheritance are the differential binding of apoE variants to the LDL receptor versus the HSPG/LRP complex and the preference of certain apoE variants for specific lipoproteins. Thus, the pathogenesis of this sometimes mysterious disorder has been clarified.  (+info)

Lipoprotein Glomerulopathy: Molecular Characterization of Three Italian Patients and Literature Survey Lipoprotein glomerulopathy (LPG) is a rare kidney disease, mainly ..
This investigation analyzed the association and interaction among APOE genotypes, various lipids including triglycerides, and the inflammatory marker CRP in a Taiwanese population. First, regarding the relationship between APOE SNPs and lipid levels, our data revealed significant associations between various genotypes or allelic combinations of the APOE SNP rs7412 and total cholesterol and LDL-C levels. Borderline significance (i.e., 0.01 , P , 0.05) was noted between various rs429358 genotypes and triglyceride, LDL-C, and HDL-C levels. Regarding the relationship between various APOE ε alleles and lipid levels, we observed significant differences in total cholesterol, LDL-C, and HDL-C levels among the carriers of the three APOE ε allele groups. In addition, when ε2 and ε4 were analyzed, we found significant differences in total cholesterol and LDL-C levels between the ε2 and non-ε2 carriers. Second, regarding the relationship between APOE and CRP, our data revealed significant associations ...
Build: Wed Jun 21 18:33:50 EDT 2017 (commit: 4a3b2dc). National Center for Advancing Translational Sciences (NCATS), 6701 Democracy Boulevard, Bethesda MD 20892-4874 • 301-435-0888. ...
Cuap car ti bantuk le cuap a hnawmmi pawl an cuap thianhnak ding caah si caah anhman mi a si bantuk in cozah sermi sii theng te ti hau lo in, mah nih fawu tein i thlawmh khawhnak sii caah a tha bak mi တောလေးညှင်း ti mi hi a si. a hmanthlak na hmuh hin lai holh in a min an theih ko lai ka zumh. lai holh in ka chim thiam ve lo mi a si caah, ca retu nih nan theihthiam ding ah kan naw hna. Mah Hnah Hi Fur ah leikuang chungah tapi hmuhkhawh mi a si. leithuang pawl caah cun hna a hnok ngai mi hramh pakhat khi a si.. ...
Type III hyperlipoproteinemia (HLP) is a genetic disorder of lipid metabolism in humans in which the primary molecular defect is a mutation(s) in apolipoprotein (apo) E that causes defective...
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Background Cardiovascular disease (CVD) is a large worldwide medical burden, with yearly increasing morbidity and mortality. An important risk factor for CVD are high cholesterol levels, with low-density lipoprotein cholesterol (LDL-C) as the main focus of research up to now. The introduction of statins has led to a great reduction ... read more in LDL-C associated risk and new agents such as ezetimibe and PCSK9 inhibitors are expected to reduce CVD risk even more. However, even in the case of low LDL-C levels, patients face residual risk. Important risk factors for residual cardiovascular risk are low levels of high-density lipoprotein (HDL) and high levels of triglyceride-rich lipoprotein (TRL). Aim This thesis aimed to investigate the relation between genetic causes of (un)favorable lipoprotein profiles, especially with regard to HDL and TRL, and several important clinical endpoints, such as diabetes mellitus (DM) and cardiovascular disease. Conclusions The causality between HDL and CVD is ...
The protein encoded by this gene is a major apoprotein of the chylomicron. It binds to a specific liver and peripheral cell receptor, and is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. This gene maps to chromosome 19 in a cluster with the related apolipoprotein C1 and C2 genes. Mutations in this gene result in familial dysbetalipoproteinemia, or type III hyperlipoproteinemia (HLP III), in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron and VLDL remnants. [provided by RefSeq, Jun 2016 ...
The protein encoded by this gene is a major apoprotein of the chylomicron. It binds to a specific liver and peripheral cell receptor, and is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. This gene maps to chromosome 19 in a cluster with the related apolipoprotein C1 and C2 genes. Mutations in this gene result in familial dysbetalipoproteinemia, or type III hyperlipoproteinemia (HLP III), in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron and VLDL remnants. [provided by RefSeq, Jun 2016 ...
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Полиморфизм гена Apo E у пациентов с метаболическим синдромом и когнитивными расстройствами
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Looking for online definition of familial dysbetalipoproteinemia in the Medical Dictionary? familial dysbetalipoproteinemia explanation free. What is familial dysbetalipoproteinemia? Meaning of familial dysbetalipoproteinemia medical term. What does familial dysbetalipoproteinemia mean?
Exogenous estrogens (ethinyl estradiol, 1 µg/kg body weight per day), which stimulate triglyceride production in normal women and those with endogenous hypertriglyceridemia, were found to exert a paradoxical, hypolipidemic effect in six subjects (five women, one man) with type III hyperlipoproteinemia on diets both of normal and of fat-free, high-carbohydrate composition. Moreover, very low-density (VLD) lipoprotein lipid and apolipoprotein composition and electrophoretic mobility became normal during estrogen administration in these subjects. Levels of normal VLD lipoproteins remained mildly to moderately elevated in a type IV lipoprotein pattern. Estrogen withdrawal promptly restored the type III pattern with its abnormal enrichment of VLD lipoproteins with apolipoprotein E (the arginine-rich peptide). These findings suggest that estrogens facilitate the assimilation of chylomicron and VLD lipoprotein remnants, a defect that appears likely to represent the metabolic abnormality underlying ...
OBJECTIVE--To elucidate the relationship, if any, between lipid abnormalities and apolipoprotein E (apo E) polymorphism, by investigating apo E phenotype and allele frequency. METHODS--Fasting blood samples were taken for determination of apo E phenotype and serum lipids in 221 male patients with gout and 141 control male subjects. Apo E phenotype was determined by one dimensional flat gel isoelectric focusing. RESULTS--Frequencies of apo E phenotypes in gout were apo E3/3 67.9%, E4/3 18.1%, E4/4 2.3%, E4/2 1.8%, E3/2 9.5%, and E2/2 0.5%; those in control male subjects were 74.5%, 15.6%, 0%, 1.4%, 7.1%, and 1.4%, respectively. Frequencies of the e2, e3, and e4 alleles in gout were 0.061, 0.817 and 0.122, compared with the corresponding control frequencies of 0.057, 0.858 and 0.085. These differences in apo E phenotype and allele frequencies between gout and control subjects were not significant. The frequency of apo e4 allele in hyperlipidaemic gout subjects was significantly greater than that ...
To study isoform-specific effects of apolipoprotein E (apoE) in vivo, we generated mice with a human APOE*2 allele in place of the mouse Apoe gene via targeted gene replacement in embryonic stem cells. Mice expressing human apoE2 (2/2) have virtually all the characteristics of type III hyperlipoprot …
Lipoprotein glomerulopathy (LPG) is a rare autosomal dominant kidney disease that is most commonly caused by mutations in ApoE Kyoto (p.R43C) and ApoE Sendai (p.R163P). Differences in phenotype among the various ApoE mutations have been suggested, but the pathogenic role of ApoE Kyoto has not been validated in an animal model. This study intended to establish an ApoE Kyoto murine model and to further compare the pathologic differences between ApoE Kyoto and ApoE Sendai. Male ApoE-deficient mice, 3 months of age, were divided into five groups, including the AD-ApoE Sendai, AD-ApoE Kyoto, AD-ApoE3, AD-eGFP, and ApoE (−/−) groups. The first four groups received recombinant adenovirus that contained the entire coding regions of the human ApoE Sendai and ApoE Kyoto, apoE3, and eGFP genes, respectively. Fasting blood and urine samples were collected at multiple time points. Lipid profiles and urine albumin-creatinine ratio were measured. Renal and aortic histopathologic alterations were analyzed. After
Apolipoprotein E (APOE) plays a major role in lipid metabolism and inflammation. However, the association between APOE gene polymorphisms and serum triglyceride levels remains controversial. We tested the effects of APOE variants on triglyceride levels and their interactions with the inflammatory marker C-reactive protein (CRP) in a Taiwanese population. Two APOE single nucleotide polymorphisms (SNPs) rs429358 and rs7412 were genotyped by TaqMan Assay using real time PCR in 595 healthy subjects attending the clinic for routine visits. After adjustment for clinical covariates, subjects carrying the rs429358-TT genotype and non-ε4 alleles were found to have higher CRP levels, whereas those with rs7412-CC genotype and non-ε2 alleles had significantly higher total and low-density lipoprotein cholesterol levels (all P | 0.01). Using subgroup and interaction analyses, we observed significantly lower triglyceride levels in subjects carrying the rs429358-TT genotype and non-ε4 alleles in the low CRP group (P
Neurology news, research and treatment studies for epilepsy, neurodegenerative disorders, patients with MS and other brain and central nervous system disorders and diseases.
...The apolipoprotein E gene ε4 allele is considered a negative fact......,A,non-invasive,,rapid,screening,method,for,Alzheimers,disease,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters
Alzheimer disease is the most common form of dementia in Western countries and the leading cause of disability in the over-65 population. Apolipoprotein E (APOE) is a multifunctional protein implied in lipid metabolism and neurobiology. Polymorphisms of the APOE gene have been associated with a vari …
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HLP Klearfold ද එම්ෙබොසිං වැනි පැහැදිලි ප්ලාස්ටික් ඇසුරුම් අපගේ ශෛලීන් සියලු බොහෝ ග්රැෆික් වැඩි දියුණු, උණුසුම් හා සිසිල් තීරු තැබීමේ, හා සෑම ඉදිරිපත් කරයි
Previous studies have demonstrated that endogenous mouse apoE is protective against transient focal and global brain ischemia and traumatic brain injury.34-36⇓⇓ Although human apoE isoforms markedly delay the appearance of Aβ deposition in APPV717F transgenic mice,14 apoE ultimately facilitates the neuritic degeneration associated with amyloid deposits and with conversion of Aβ into mature fibrillar amyloid,15 which is thought to be neurotoxic.37 In the present study, we show that neuronal overexpression of human APP751 at the level detected in early AD and Downs syndrome28 dramatically increases the susceptibility to ischemic brain damage in the absence of apoE. Moreover, expression of human apoE3 or apoE4 in astrocytes significantly reduces the neuronal vulnerability to ischemia in APP751 transgenic mice. These results indicate that even though apoE may be a contributory factor in Aβ-induced toxicity in AD, it has a beneficial role against APP751-induced ischemic vulnerability. ...
Results from two small studies, involving a total of only 174 cases, have suggested that the increased risk of coronary heart disease conferred by cigarette smoking is substantially affected by genotype at the apolipoprotein E (APOE) epsilon2/epsilon3/epsilon4 polymorphism. We have established APOE genotypes in 4484 patients with acute myocardial infarction diagnosed before the age of 55 years for male and 65 years for female patients, and in 5757 controls with no history of cardiovascular disease. On average, the hazard ratio for myocardial infarction was 1.17 (95% CI 1.09-1.25; p|0.00001) per stepwise change from epsilon3/2 to epsilon3/3 to epsilon3/4 genotype. Among individuals in this study with known cigarette smoking status, the hazard ratio for myocardial infarction in smokers versus non-smokers was 4.6 (4.2-5.1). There was, however, no significant difference between the smoker/non-smoker hazard ratios for those with different APOE genotypes (chi2(2)=0.69; p=0.7). When differences in risk between
Relchap:Magway ramthen,Minbu (မင်းဘူး)peng, pengkomh palik sakhan cu mipi vengtu phu hna nih nizaan ah luhhnawh in an doh hna caah kaphnih kar kahdohnak a chuak, palik cheukhat hliam an tuar tiah mipi vengtu phu hna nih an langhter.. Minbu(မင်းဘူး) mipi vengtu phu in thawngzamhnak nawlngei tu pakhat nih zaan ah sakhan cu bomb pahnih in kan cheh, pakhat a puak. Bomb cu kut ser mi bomb a si lo, bomb cu a puah caah sakhan chung in meithal an puah chih.. Kanmah zong hmunhma kan lak nak hmun in kan kah ve hna cun hnu kan tolh.Kanmah lei in hliamtuar mi an um lo.Palik sakhan he neihniam mi hna chim nak ahcun anmah lei ah hliam tuar mi an um tiah theih a si.. Minbu (မင်းဘူး) khua chungah ralhrang phu hna nih, atulio ah minung thazaang chap in mipi hna sin ah phaisa hal in le checkhlatnak cu tu le tu ah tuah caah Minbu khuachung no.4 sang pengkomh palik sakhan cu luhhnawh in kah a si tiah thawngchim nak nawl ngei tu pakhat nih achim.. Nihin zinglei ah Minbu ...
Buy anti-APOE antibody, anti-Mouse Apolipoprotein E (Apo E) Polyclonal Antibody-P02649.1 (MBS315478) product datasheet at MyBioSource, Primary Antibodies. Application: DD, IEP, RID, Western Blot
Effective immediately, SpectraCell Laboratories now offers apolipoprotein E genotyping. This test determines a persons genetic risk for heart disease associated with the commonly
Health, ...MONDAY March 7 (HealthDay News) -- Genetics may predispose some peopl...The culprit is a specific abnormality of the apolipoprotein E gene. Th...Now a team of researchers led by Brian K. Lee of Drexel University in...The observation is reported in the March issue of the Archives of ...,Mix,of,Genetics,and,Stress,Can,Impair,Mental,Abilities,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
ApoE belongs to a group of proteins that bind reversibly with lipoprotein and play an important role in lipid metabolism.  In addition
Amarin announced that it has reached agreement with the U.S. FDA under a Special Protocol Assessment for its planned Phase 3 clinical trial of AMR101 in patients with mixed dyslipidemia.
Associations between apolipoprotein E genotypes and serum levels of glucose, cholesterol, and triglycerides in a cognitively normal aging Han Chinese population Qing-Qing Tao,1,* Yan Chen,2,3,* Zhi-Jun Liu,1 Yi-Min Sun,1 Ping Yang,1 Shen-Ji Lu,1 Miao Xu,1 Qin-Yun Dong,1 Jia-Jun Yang,2 Zhi-Ying Wu11Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, 2Department of Neurology, Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, 3Department of Medicine, Shanghai Fengxian District Central Hospital, Shanghai, People’s Republic of China*These authors contributed equally to this workPurpose: To determine the associations between apolipoprotein E (APOE) genotypes and serum levels of glucose, total cholesterol, and triglycerides in a cognitively normal aging Han Chinese population.Methods: There were 1,003 cognitively normal aging subjects included in this study. APOE genotypes were analyzed and biochemical
Meckes, C., Moyna, N., Tsongalis, G., Miles, M. (2001). Apolipoprotein E Genotype Does Not Affect the Changes in Serum Lipids with Exercise Training. Circulation, 104(17), 343-343 ...
Accumulation of β-amyloid (Aβ) in the brain is essential to Alzheimers disease (AD) pathogenesis. Carriers of the apolipoprotein E (APOE) ε4 allele demonstrate greatly increased AD risk and enhanced brain Aβ deposition. In contrast, APOE ε2 allele carries show reduced AD risk, later age of disease onset, and lesser Aβ accumulation. However, it remains elusive whether the apoE2 isoform exerts truly protective effect against Aβ pathology or apoE2 plays deleterious role albeit less pronounced than the apoE4 isoform. Here, we characterized APPSW/PS1dE9/APOE ε2-TR (APP/E2) and APPSW/PS1dE9/APOE ε4-TR (APP/E4) mice, with targeted replacement (TR) of the murine Apoe for human ε2 or ε4 alleles, and used these models to investigate effects of pharmacological inhibition of the apoE/Aβ interaction on Aβ deposition and neuritic degeneration. APP/E2 and APP/E4 mice replicate differential effect of human apoE isoforms on Aβ pathology with APP/E4 mice showing a several-fold greater load of Aβ plaques,
Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with vascular amyloid deposition.
Xu PT, Schmechel D, Rothrock-Christian T, et al. () Human apolipoprotein E2, E3, and E4 isoform-specific transgenic mice: human-like pattern of glial and neuronal immunoreactivity in central nervous system not observed in wild-type mice. Neurobiol Dis - PubMed CrossRef Google ScholarCited by: 1.
OBJECT: The presence of the apolipoprotein E-epsilon4 (APOE-epsilon4) allele is reported to be associated with poor outcome after traumatic brain injury (TBI). This study was performed to determine if the presence of the APOE-epsilon4 allele influenced outcome in a cohort of black patients with TBI
FITC偶联Apolipoprotein E 抗体(ab27613)可与人样本反应并经ICC/IF实验严格验证,实验条件参看说明书。Abcam对所有产品均提供质保服务和专属技术支持,中国75%以上现货。
OBJECTIVE:To investigate the association between the apolipoprotein E (APOE) genotypes and dementia in patients with stroke, defined as either vascular dementia (VaD) or Alzheimer disease with cerebrovascular disease (AD with CVD). DESIGN AND SETTING:Population-based, case-control study from Rotterdam, the Netherlands, and New York City. PARTICIPANTS:A total of 187 patients with dementia and stroke were compared with 507 controls similar in age and ethnic group. MAIN OUTCOME MEASURES:The APOE allele frequencies in patients and controls; the odds ratio of dementia with stroke, VaD, and AD with CVD, adjusted for age, sex, residency, and education; and the percent attributable risk related to the APOE epsilon4 allele. RESULTS:Overall, patients with dementia and stroke had a higher APOE epsilon4 allele frequency than controls. Compared with APOE epsilon3 homozygote individuals, APOE epsilon4 homozygotes had a 7-fold increased risk of dementia with stroke (OR=6.9; 95% CI, 1.6-29.4), while APOE epsilon4
APOE epsilon4 is the best-established genetic risk factor for sporadic Alzheimers disease (AD). However, while homozygotes show greater disease susceptibility and earlier age of onset than heterozygotes, they may not show faster rates of clinical progression. We hypothesize that there are differential APOE epsilon4 allele-load dependent influences on neuropathology across the brain. Our aim was to define the relationship between APOE epsilon4 allele load and regionally-specific brain cortical atrophy in Alzheimers Disease (AD). For this reason voxel-based morphometry (VBM) was performed using T1-weighted MR images from 83 AD patients, contrasting regional cortical grey matter by APOE epsilon4 load according to either dominant or genotypic models. Patients fulfilled NINCDS-ADRDA criteria and were genotyped for APOE epsilon4 (15 epsilon4/epsilon4, 39 epsilon4/- and 29-/-). We observed that grey matter volume (GMV) decreased additively with increasing allele load in the medial (MTL) and anterior temporal
The human APOE gene, which codes for apolipoprotein E (apoE), has three major polymorphic alleles: ε2, ε3, and ε4 that give rise to amino acid substitutions. APOE-ε4 is a strong risk factor of sporadic Alzheimers disease (AD) but the reason why is still unknown despite intense research for more than 20 years. The aim of the study was to investigate if the concentrations of total apoE and the specific apoE isoforms in cerebrospinal fluid (CSF) differ between various neurodegenerative diseases and control individuals, as well as among the APOE genotypes. Quantification of total apoE and specific apoE isoforms (E2, E3, and E4) in CSF was performed using high-resolution parallel reaction monitoring mass spectrometry. In total, 1820 individuals were involved in the study including clinically diagnosed AD patients (n = 228), cognitively unimpaired (CU) patients (n = 896), and patients with other neurodegenerative disorders (n = 696). Follow-up data was available for 100 individuals, assessed at two time
Application of uniform methods for measuring the apolipoprotein (apo) E polymorphism and plasma cholesterol levels in nine populations (Tyrolean, Sudanese, Indian, Chinese, Japanese, Hungarian, Icelandic, Finnish, and Malay) revealed significant heterogeneity among them in apo E type frequencies and mean cholesterol levels. The major apo E types in all populations were E3/2 (frequency range from 7.0% in Indians to 16.9% in Malays), E3/3 (frequency range from 39.8% in Sudanese to 72.1% in Japanese), and E3/4 (frequency range from 11.3% in Japanese to 35.9% in Sudanese). Mean cholesterol levels ranged from 144.2 mg/dl in the Sudanese to 228.5 mg/dl in the Icelandics. Two-way analysis of variance of the effect of population and apo E type on cholesterol levels showed no significant interaction effect, indicating that the effects of apo E type on cholesterol levels do not differ significantly among the populations. The overall average excess for the ε2 allele was -14.12 mg/dl (range -31.63 to -8.82 ...
ABSTRACT. Alzheimer disease (AD) is a progressive and irreversible neurodegenerative disorder that is characterized by cognitive decline, memory loss and confusion. The E4 allele of the apolipoprotein E gene (APOE) is associated with AD and it is the main genetic risk factor for disease. Although the exact physiological function is unknown, bleomycin hydrolase (BLMH) may also be associated with AD development, although previous immunohistochemical findings have been inconsistent. Therefore, the purpose of this study was to evaluate the genotypic and allele frequencies of the APOE gene and BLMH 1450 G > A polymorphism and assess BLMH expression using PCR-RFLP and RT-qPCR analyses of blood samples from patients with Alzheimer disease (AD), healthy elderly adults (EC) and healthy young subjects (YC). BLMH expression was significantly different among groups (p = 0.015) and there was substantial reduction with age and with AD. The APOE and BLMH genotype frequency did not diverge from the ...
Introduction : The focus of this study was to assess cognitive functions in relation to androgens and specifically testosterone and dehydroepiandrosterone in postmenopausal women as well as the correlation between cognitive functions and these two androgens according to polymorphism of the...
Fingerprint Dive into the research topics of Physiological relevance of apolipoprotein E recycling: Studies in primary mouse hepatocytes. Together they form a unique fingerprint. ...
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Amino Acid SequenceMHHHHHHKVE QAVETEPEPE LRQQTEWQSG QRWELALGRF WDYLRWVQTL SEQVQEELLS SQVTQELRAL MDETMKELKA YKSELEEQLT PVAEETRARL SKELQAAQAR LGADMEDVRG RLVQYRGEVQ AMLGQSTEEL RVRLASHLRK LRKRLLRDAD DLQKRLAVYQ AGAREGAERG LSAIRERLGP LVEQGRVRAA TVGSLAGQPL QERAQAWGER LRARMEEMGS RTRDRLDEVK EQVAEVRAKL EEQAQQIRLQ AEAFQARLKS WFEPLVEDMQ RQWAGLVEKV QAAVGTSAAP VPSDNH.DescriptionApolipoprotein E4 Human Recombinant produced in E.coli is a single, non-glycosylated polypeptide chain containing a total of 306 amino acids including a His Tag at N-terminus and having a molecular mass of 35.2kDa. The Accession # is P02649 VAR_000652.FormulationLyophilized from a sterile (0.2µm) filtered aqueous solution containing 10mM sodium phosphate, pH 7.5.Physical AppearanceSterile Filtered White lyophilized (freeze-dried) powder.PurityGreater than 90% as determined by SDS-PAGE.SolubilityIt is recommended to reconstitute the lyophilized APOE4 in sterile 18M-cm H2O not less than 100µg/ml, which can then be further diluted to other
Mouse Monoclonal Anti-Apolipoprotein E/ApoE Antibody (WUE-4) [DyLight 650]. Validated: WB, ELISA, Flow, ICC/IF, IHC. Tested Reactivity: Human, Mouse. 100% Guaranteed.
Epsilon polymorphism of apolipoprotein E gene and insertion-deletion polymorphism of ACE gene and brain ischemic stroke in children: association pilot-study ...
Researchers have identified a protein called apolipoprotein E (ApoE) which affects your chances of developing Alzheimers disease. There are three forms of ApoE: ApoE2, ApoE3 and ApoE4.. Having one or two copies of ApoE4 increases someones chance of developing the disease, but does not make it certain. Some researchers think that ApoE4 does not affect whether a person will get the disease but, rather, when they get it, causing people with ApoE4 to develop the disease before people with ApoE2.. ...
The ApoE gene may have a more influential role than first thought; it may amplify the damage done by the tau protein, causing neurodegeneration.
Pam speaks throughout the country at lectures and seminars about the APO E Gene Program and health. To find out more information about attending any of her appearances or having her speak at an event, please contact the office at (925) 736-8510.. ...
All members of this family are receptors for Apolipoprotein E (ApoE). Therefore, they are often synonymously referred to as ' ... ApoE receptors'. ApoE occurs in 3 common isoforms (E2, E3, E4) in the human population. ApoE4 is the primary genetic risk ... Andersen OM, Benhayon D, Curran T, Willnow TE (August 2003). "Differential binding of ligands to the apolipoprotein E receptor ... Herz J, Beffert U (October 2000). "Apolipoprotein E receptors: linking brain development and Alzheimer's disease". Nature ...
E1 and E2 are covalently bonded when embedded in the envelope of HCV and are stabilized by disulfide bonds. E2 is globular and ... Recent research indicates that these apolipoproteins interact with scavenger receptor B1 (SR-B1). SR-B1 is able to remove ... E1 serves as the fusogenic subunit and E2 acts as the receptor binding protein. E1 has 4-5 N-linked glycans and E2 has 11 N- ... In addition, E2 can shield E1 from the immune system. Although HVR1 is quite variable in amino acid sequence, this region has ...
Also, research has been put on concerning apolipoprotein E genotypes; this polymorphism has three alleles (*e2, *e3, and *e4) ... Specifically too, the apolipoprotein *e4 allele is linked to Alzheimer's disease as well. Also, there is increased coronary ...
1992). "Site-directed mutagenesis and structure-function analysis of the human apolipoprotein A-I. Relation between lecithin- ... 1992). "Interaction of rat lecithin-cholesterol acyltransferase with rat apolipoprotein A-I and with lecithin-cholesterol ...
"Genetic Study of Low-Density Lipoprotein Receptor Gene and Apolipoprotein B-100 Gene among Malaysian Patients with Familial ...
Martineau, C; Najyb, O; Signor, C; Rassart, É; Moreau, R (September 2016). "Apolipoprotein D deficiency is associated to high ... Identification of apolipoprotein D, apolipoprotein A-IV, apolipoprotein E, and apolipoprotein A-I". The Journal of Biological ... "Entrez Gene: APOD apolipoprotein D". Muffat J, Walker DW (January 2010). "Apolipoprotein D: an overview of its role in aging ... Apolipoprotein D (Apo-D) is a component of high-density lipoprotein that has no marked similarity to other apolipoprotein ...
... of the APOE3 gene created the E2 allele. The gene, APOE, is mapped to chromosome 19 in a cluster with apolipoprotein C1 (APOC1 ... "Entrez Gene: APOE apolipoprotein E". Liu CC, Liu CC, Kanekiyo T, Xu H, Bu G (February 2013). "Apolipoprotein E and Alzheimer ... "Genetic studies of human apolipoproteins. X. The effect of the apolipoprotein E polymorphism on quantitative levels of ... Apolipoprotein E (APOE) is a protein involved in the metabolism of fats in the body of mammals. A subtype is implicated in ...
... intronic variant is significantly associated with decreased risk of Alzheimer's disease in males carrying an apolipoprotein E ...
Maternal apolipoprotein E has also been implicated in individual variability in SLOS, although the exact nature of this ...
The apolipoprotein B (apoB) 5′ UTR cis regulatory element is an RNA element located in the 5′ UTR of the human apoB mRNA. This ... Page for Apolipoprotein B (apoB) 5′ UTR cis-regulatory element at Rfam v t e. ... Pontrelli L, Sidiropoulos KG, Adeli K (June 2004). "Translational control of apolipoprotein B mRNA: regulation via cis elements ...
... de ditos pacientes son E2/E2, mentres que só ∼2% dos E2/E2 desenvolven a doenza, polo que é probable que estean implicados ... "Entrez Gene: APOE apolipoprotein E".. *↑ Liu CC, Liu CC, Kanekiyo T, Xu H, Bu G (Feb 2013). "Apolipoprotein E and Alzheimer ... As persoas cunha combinación homocigótica E2/E2 só poden eliminar a graxa da dieta lentamente e teñen un maior risco de ter ... en relación co E2 e E3) é unha asociacion positiva con niveis altos de vitamina D, que pode axudar a explicar a súa prevalencia ...
... the apolipoprotein E receptor type 2 (ApoER2), and the cytoplasmic adapter protein disabled 1 (Dab1). In early cortical ...
PDB: 1RW6​; Wang Y, Ha Y (Aug 2004). "The X-ray structure of an antiparallel dimer of the human amyloid precursor protein E2 ... Barger SW, DeWall KM, Liu L, Mrak RE, Griffin WS (Aug 2008). "Relationships between expression of apolipoprotein E and beta- ... The hypothesis that APP has ferroxidase activity in its E2 domain and facilitates export of Fe(II) is possibly incorrect since ... The extracellular region, much larger than the intracellular region, is divided into the E1 and E2 domains, linked by an acidic ...
"Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis". Nature ... 126 (4): 722-729.e2. doi:10.1016/j.jaci.2010.05.046. PMID 20673980.. ...
... and apolipoprotein A-I: significance for cardiovascular risk: the IDEAL and EPIC-Norfolk studies". J. Am. Coll. Cardiol. 51 (6 ...
En tamaño, a HDL é a menor das partículas de lipoproteínas. Tamén é a máis densa porque contén a maior proporción de proteínas ... of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins ... A HMG-CoA redutase é un importante encima no metabolismo do colesterol e lípidos, pero non é o único. As estatinas actúan ... Nos humanos, probablemente a vía máis importante é a indirecta, a cal é mediada pola proteína de transferencia de colesteril ...
Tognon G. Non é vero ma credici! Le bugie sulla corretta alimentazione e i consigli per scegliere alimenti di qualità (It's not ... Comparison of Apolipoprotein (apoB/apoA-I) and Lipoprotein (Total 2 Cholesterol/HDL) Ratio Determinants. Focus on Obesity, Diet ... Diet Score and Mortality Are Inversely Associated in Adults Living in the Subarctic Region Comparison of Apolipoprotein (apoB/ ...
126 (4): 722-729.e2. doi:10.1016/j.jaci.2010.05.046. PMID 20673980. Engels, F; Kessels, G. C; Henricks, P. A; Nijkamp, F. P ( ... "Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis". Nature ...
67 (4): 423-432.e2. doi:10.1016/j.annemergmed.2015.08.019. ISSN 0196-0644. PMC 4808407. PMID 26440490. Almoallim, Hani (2016). ... "Effect of Replacing Race With Apolipoprotein L1 Genotype in Calculation of Kidney Donor Risk Index". American Journal of ...
... modulates C to U editing of apolipoprotein B mRNA by interacting with apobec-1 and ACF, the apobec-1 complementation ... 2004). "Dynamic antagonism between RNA-binding protein CUGBP2 and cyclooxygenase-2-mediated prostaglandin E2 in radiation ... CUGBP2 modulates C to U editing of apolipoprotein B mRNA by interacting with apobec-1 and ACF, the apobec-1 complementation ...
... the most common cause for this form is the presence of ApoE E2/E2 genotype. It is due to cholesterol-rich VLDL (β-VLDL). Its ... The lipoprotein density and type of apolipoproteins it contains determines the fate of the particle and its influence on ... Online Mendelian Inheritance in Man (OMIM): Apolipoprotein C-II Deficency - 207750 Yamamura T, Sudo H, Ishikawa K, Yamamoto A ( ... or altered apolipoprotein C2, resulting in elevated chylomicrons, the particles that transfer fatty acids from the digestive ...
Nahmias Y, Goldwasser J, Casali M, van Poll D, Wakita T, Chung RT, Yarmush ML (May 2008). "Apolipoprotein B-dependent hepatitis ... doi:10.1023/B:BREA.0000025397.56192.e2. ISSN 0167-6806. PMID 15111768. S2CID 24436665. Ferreira, Ricardo J; Baptista, Rafael; ... apolipoprotein B overproduction, and hyperinsulinemia in LDL receptor-null mice with diet-induced insulin resistance". Diabetes ...
If estradiol (E2) levels are sufficient, NPY induces GnRH secretion. Amenorrheic women have been found to have lower serum NPY ... In an interesting position between these two alternatives, elevations in total cholesterol, LDLc, apolipoprotein B, and ... Estradiol (E2), an estrogen steroid hormone and the major female sex hormone, has a cardio-protective effect. As such, ... Short-term use of transdermal estradiol E2 with cyclic oral progestin may be used for estrogen replacement. Care must be taken ...
... and an E2-binding site". Proc. Natl. Acad. Sci. U.S.A. 103 (2): 341-6. Bibcode:2006PNAS..103..341C. doi:10.1073/pnas.0506618103 ... results in increased ubiquitinylation and decreased secretion of apolipoprotein B100 in HepG2 cells". J. Biol. Chem. 278 (26): ...
Hung HL, Kim AY, Hong W, Rakowski C, Blobel GA (April 2001). "Stimulation of NF-E2 DNA binding by CREB-binding protein (CBP)- ... "CREB-binding protein is a transcriptional coactivator for hepatocyte nuclear factor-4 and enhances apolipoprotein gene ...
Amrine-Madsen, H.; Koepfli, K.P.; Wayne, R.K.; Springer, M.S. (2003). "A new phylogenetic marker, apolipoprotein B, provides ... 30 (7): 1346-1351.e2. doi:10.1016/j.cub.2020.03.022. PMC 7156161. PMID 32197085. "Civet Cat Slaughter To Fight SARS". CBSNews. ...
Study have shown that ABCA1 mediates transport of cholesterol from peripheral tissues to Apolipoprotein-1 and it is also ... 124 (9): 841-51.e2. doi:10.1016/j.amjmed.2011.04.024. PMID 21854893. "Unit 6: Cardiovascular, Circulatory, and Hematologic ... Apolipoprotein E)-Deficient Mouse Atherosclerosis". Arteriosclerosis, Thrombosis, and Vascular Biology. 39 (5): 876-887. doi: ... Apolipoprotein E)-Deficient Mouse Atherosclerosis". Arteriosclerosis, Thrombosis, and Vascular Biology. 39 (5): 876-887. doi: ...
Estudos feitos con ratos transxénicos indican que a calreticulina é ademais un xene embrionario cardíaco que é esencial durante ... "Gene-centric Association Signals for Lipids and Apolipoproteins Identified via the HumanCVD BeadChip". Am. J. Hum. Genet. 85 ... A calreticulina é unha proteína multifuncional que se une ao Ca2+ (un segundo mensaxeiro na transdución de sinais), facéndoo ... O termo "mobilferrina"[3] tamén se considera que é equivalente a calreticulina por algunhas fontes.[4] ...
Apolipoprotein E (ApoE) has been shown to be an important and common factor in CNS responses. ApoE controls the redistribution ... COX-2 up-regulation in irradiated microglia cells leads to prostaglandin E2 production, which appears to be responsible for ...
... research has been put on concerning apolipoprotein E genotypes; this polymorphism has three alleles (*e2, *e3, and *e4)and was ... Specifically too, the apolipoprotein *e4 allele is linked to Alzheimer's disease as well. Also, there is increased coronary ...
Apolipoprotein E, Dementia, and Cortical Deposition of Beta-amyloid Protein. The New England Journal of Medicine. 1995;333(19): ... juni 2010;123(6):522-527.e2. doi:10.1016/j.amjmed.2010.01.017. PMID 20569758. ... a b Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease. Proceedings ... Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial ...
apolipoprotein A-I receptor binding. • GTP-dependent protein binding. • GTPase activity. • mitogen-activated protein kinase ...
74.0 74.1 Mahley RW, Weisgraber KH, Huang Y (Aprili 2006). "Apolipoprotein E4: a causative factor and therapeutic target in ... 522-527.e2. doi:10.1016/j.amjmed.2010.01.017 . ... "Apolipoprotein E: high-avidity binding to beta-amyloid and ... Polvikoski T, Sulkava R, Haltia M, et al. (Novemba 1995). "Apolipoprotein E, dementia, and cortical deposition of beta-amyloid ...
"Very early changes in olfactory functioning due to Alzheimer's disease and the role of apolipoprotein E in olfaction". Annals ...
... a specific isoform of apolipoprotein, APOE4, is a major genetic risk factor for AD. While apolipoproteins enhance the breakdown ... 123 (6): 522-527.e2. doi:10.1016/j.amjmed.2010.01.017. PMID 20569758.. ... The best known genetic risk factor is the inheritance of the ε4 allele of the apolipoprotein E (APOE).[44][45] Between 40 and ... "Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein". The New England Journal of Medicine. 333 (19): ...
A esperança de vida da população com Alzheimer é reduzida.[210][211][212] A esperança média de vida após o diagnóstico é de ... Xu H, Finkelstein DI, Adlard PA (12 de junho de 2014). «Interactions of metals and Apolipoprotein E in Alzheimer's disease». ... Alzheimer é uma doença terminal, em que a causa direta de morte não é a doença em si, mas geralmente um fator externo, como uma ... Nos indivíduos com oito anos ou mais de escolaridade a prevalência é de 3,5%, enquanto que nos analfabetos é de 12,2%.[220] ...
1995). «Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein». N Engl J Med. 333 (19): 1242-47. PMID ... 123 (6): 522-527.e2. PMID 20569758. doi:10.1016/j.amjmed.2010.01.017.. CS1-vedlikehold: Flere navn: forfatterliste (link) ... Den mest kjente genetiske risikofaktoren er arv av ε4-allelet av apolipoprotein E (APOE).[74][75] Mellom 40 og 80 % av ... 1993). «Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial ...
The American Journal of Medicine". 123 (6), s. 522-527.e2, June 2010. DOI: 10.1016/j.amjmed.2010.01.017. PMID: 20569758. ... Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein. „N Engl J Med". 333 (19), s. 1242-47, 11 1995. DOI ... Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial ... a b Mahley RW, Weisgraber KH, Huang Y. Apolipoprotein E4: A causative factor and therapeutic target in neuropathology, ...
... isoform spesifik apolipoprotein, APOE4, adalah faktor risiko genetik utama untuk Alzheimer. Walaupun apolipoprotein ... 123 (6): 522-527.e2. doi:10.1016/j.amjmed.2010.01.017. PMID 20569758.. ... Faktor risiko genetik yang paling terkenal adalah pewarisan alel ε4 apolipoprotein E (APOE).[44][45] Antara 40 dan 80% orang ... "Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein". The New England Journal of Medicine. 333 (19): ...
2010-06, 123 (6): 522-27.e2. PMID 20569758. doi:10.1016/j.amjmed.2010.01.017 (英语).. ... Interactions of metals and Apolipoprotein E in Alzheimer's disease. Frontiers in Aging Neuroscience. 2014-06-12, 6: 121. PMC ... Strittmatter WJ, Saunders AM, Schmechel D. Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of ... Polvikoski T, Sulkava R, Haltia M. Apolipoprotein E, Dementia, and Cortical Deposition of Beta-amyloid Protein. The New England ...
2 E2,2 54.13 cM. Start. 102,811,141 bp[2]. End. 102,901,665 bp[2]. ...
MeSH D12.776.070.400.200.100 - apolipoprotein A1 MeSH D12.776.070.400.200.150 - apolipoprotein A2 See List of MeSH codes ( ... adenovirus e2 proteins MeSH D12.776.624.664.520.045.070 - adenovirus e3 proteins MeSH D12.776.624.664.520.045.080 - adenovirus ... adenovirus e2 proteins MeSH D12.776.964.700.045.070 - adenovirus e3 proteins MeSH D12.776.964.700.045.080 - adenovirus e4 ...
ɛ2 allele.Design:Controlled, parallel study.Subjects:There were 15 subjects with the apolipoprotein E (APOE)3/2 genotype and ... Apolipoprotein E genotypes and their relation to lipid levels in a rural South African population. Masemola, Matshane L.; ... Influence of the Apolipoprotein E Polymorphism on Plasma Lipoproteins in a Mexican Population. Gamboa, Ricardo; Vargas-Alarcon ... Associations between Apolipoprotein E Genotype, Diet, Body Mass Index, and Serum Lipids in Lithuanian Adult Population. ...
... possible association with apolipoprotein E2 isoform. J Lipid Res 1994;35:1066-1075PMID : 8077845.. ... Type III hyperlipoproteinemia: defective metabolism of an abnormal apolipoprotein E. Science 1981;211:584-586PMID : 7455696.. ... The effect of partial LPL deficiency and dysbetalipoproteinemia can be modulated by other genes, such as apolipoprotein (apo) E ... Dietary fat clearance in normal subjects is regulated by genetic variation in apolipoprotein E. J Clin Invest 1987;80:1571- ...
Intracerebral adeno-associated virus gene delivery of apolipoprotein E2 markedly reduces brain amyloid pathology in Alzheimers ... Intracerebral adeno-associated virus gene delivery of apolipoprotein E2 markedly reduces brain amyloid pathology in Alzheimers ... The common apolipoprotein E alleles (ε4, ε3, and ε2) are important genetic risk factors for late-onset Alzheimers disease, ... Preclinical and clinical studies have shown that apolipoprotein E (APOE) genotype also predicts the timing and amount of brain ...
Human apolipoprotein E has three isoforms: APOE2, APOE3 and APOE41. APOE4 is a major genetic risk factor for Alzheimers ... Associations of APOE e2 genotype with cerebrovascular pathology: a postmortem study of 1275 brains *Terry E Goldberg ... Human apolipoprotein E has three isoforms: APOE2, APOE3 and APOE41. APOE4 is a major genetic risk factor for Alzheimers ... Apolipoprotein E controls cerebrovascular integrity via cyclophilin A. *Robert D. Bell1,2. , ...
E2 allele of the apolipoprotein E gene polymorphism is predictive for obesity status in Roma minority population of Croatia ... E2 allele of the apolipoprotein E gene polymorphism is predictive for obesity status in Roma minority population of Croatia ... Association of apolipoprotein E genetic variation in Alzheimers disease in Indian population: a meta-analysis. Agarwal R, ... The presence of apolipoprotein epsilon4 and epsilon2 alleles augments the risk of coronary artery disease in type 2 diabetic ...
Martineau, C; Najyb, O; Signor, C; Rassart, É; Moreau, R (September 2016). "Apolipoprotein D deficiency is associated to high ... Identification of apolipoprotein D, apolipoprotein A-IV, apolipoprotein E, and apolipoprotein A-I". The Journal of Biological ... "Entrez Gene: APOD apolipoprotein D". Muffat J, Walker DW (January 2010). "Apolipoprotein D: an overview of its role in aging ... Apolipoprotein D (Apo-D) is a component of high-density lipoprotein that has no marked similarity to other apolipoprotein ...
Apolipoprotein E2. Grant support. *K23 NS059774/NS/NINDS NIH HHS/United States ...
Apolipoprotein E (ApoE): E2/E3/E4. DGKL 2 (RfB) 12 ECAT7 (in collaboration with DGKL). ...
1996) Human apolipoprotein E2, E3, and E4 isoform-specific transgenic mice: human-like pattern of glial and neuronal ... Apolipoproteins E3 and E2 greater than E4. J Biol Chem 273:13452-13460. ... 1991) Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation. J Clin Invest 88:270-281. ... 1995a) Macrophage-specific expression of human apolipoprotein E reduces atherosclerosis in hypercholesterolemic apolipoprotein ...
Apolipoprotein E2 transgenic rabbits. Modulation of the type III hyperlipoproteinemic phenotype by estrogen and occurrence of ... Corbo RM, Scacchi R. Apolipoprotein E (APOE) allele distribution in the world. Is APOE*4 a thrifty allele?. Ann Hum Genet. ... Apolipoprotein E polymorphism and atherosclerosis. Arteriosclerosis. 1988 Jan-Feb. 8(1):1-21. [Medline]. ... Smelt AH, de Beer F. Apolipoprotein E and familial dysbetalipoproteinemia: clinical, biochemical, and genetic aspects. Semin ...
Reln is part of a signal transduction pathway that includes the apolipoprotein E2 (ApoER2), the very low-density lipoprotein ...
Apolipoprotein E2 / genetics*. Apolipoprotein E4 / genetics*. Brain Ischemia / etiology. Cerebral Infarction / etiology. Female ... RESULTS: Apolipoprotein E epsilon2 or epsilon4-containing genotypes were not associated with outcome, occurrence of cerebral ...
Nuclear factor-E2-related factor 2. OXPHOS. Oxidative phosphorylation. PERK. Eukaryotic translation initiation factor-2α kinase ... 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 ...
Protective effect of apolipoprotein E2 on coronary artery disease in African Americans is mediated through lipoprotein ... Protective effect of apolipoprotein E2 on coronary artery disease in African Americans is mediated through lipoprotein ... Protective effect of apolipoprotein E2 on coronary artery disease in African Americans is mediated through lipoprotein ... Protective effect of apolipoprotein E2 on coronary artery disease in African Americans is mediated through lipoprotein ...
Apolipoprotein E2 transgenic rabbits. Modulation of the type III hyperlipoproteinemic phenotype by estrogen and occurrence of ... Corbo RM, Scacchi R. Apolipoprotein E (APOE) allele distribution in the world. Is APOE*4 a thrifty allele?. Ann Hum Genet. ... Apolipoprotein E polymorphism and atherosclerosis. Arteriosclerosis. 1988 Jan-Feb. 8(1):1-21. [Medline]. ... Smelt AH, de Beer F. Apolipoprotein E and familial dysbetalipoproteinemia: clinical, biochemical, and genetic aspects. Semin ...
Apolipoprotein E2 transgenic rabbits. Modulation of the type III hyperlipoproteinemic phenotype by estrogen and occurrence of ... Corbo RM, Scacchi R. Apolipoprotein E (APOE) allele distribution in the world. Is APOE*4 a thrifty allele?. Ann Hum Genet. ... Apolipoprotein E polymorphism and atherosclerosis. Arteriosclerosis. 1988 Jan-Feb. 8(1):1-21. [Medline]. ... Smelt AH, de Beer F. Apolipoprotein E and familial dysbetalipoproteinemia: clinical, biochemical, and genetic aspects. Semin ...
Protective role of the apolipoprotein E2 allele in age-related disease traits and survival: evidence from the Long Life Family ... Protective role of the apolipoprotein E2 allele in age-related disease traits and survival: Evidence from the Long Life Family ... The apolipoprotein E (apoE) is a classic example of a gene exhibiting pleiotropism. We examine potential pleiotropic ...
Acute Disease , Adult , Apolipoprotein E2/genetics , Apolipoprotein E3/genetics , Biomarkers/blood , Combined Modality Therapy ... hyperlipidemia and acute pancreatitis with underlying partial lipoprotein lipase deficiency and apolipoprotein E3/E2 genotype ... deficiency but without an associated LPL gene mutation in the presence of the apolipoprotein E3/2 genotype. This is the first ... extreme gestational hyperlipidemia with a partial LPL deficiency in the absence of an LPL gene mutation and the apolipoprotein ...
Human apolipoprotein E2 promotes parenchymal amyloid deposition and neuronal loss in vasculotropic mutant amyloid-β protein Tg- ... Human apolipoprotein E2 promotes parenchymal amyloid deposition and neuronal loss in vasculotropic mutant amyloid-β protein Tg- ... Human apolipoprotein (ApoE) genotype influences the development of Alzheimers disease and cerebral amyloid angiopathy (CAA), ...
Characterization of Three Human Apolipoprotein E Isoforms (E2, E3 and E4) Expressed in Escherichia coli Barbier, Anne / ...
... the ApoE genotypes were pooled in groups containing the haplotype e2 (e2/e2 and e2/e3), haplotype e3 only, and haplotype e4 (e3 ... While the e2 isoform in newborns is associated with elevated maternal LDL-C and apolipoprotein B (ApoB) levels, the same ... Apolipoprotein E (ApoE) and its isoforms (e2, e3, and e4) are involved in the regulation of lipid metabolism. Specifically, ... show a significant effect on the birth weight percentiles in any of the analyzed subgroups compared to the groups e2/e2 and e2/ ...
... apolipoprotein C1, nos povos da ascendência americana do indiano e do mexicano que é ligada ao ... Apolipoprotein C1 é um componente da lipoproteína high-density (HDL) e da lipoproteína da baixa densidade (LDL). O colesterol ... A proteína de Apolipoprotein C1 ligou a BMI elevado nos povos da ascendência americana do indiano e do mexicano. *Download PDF ... Aviso: Esta página é uma tradução automática da página original em inglês. Por favor note uma vez que as traduções são geradas ...
immunogen = human apolipoprotein E. reacts to the E2, E3 and E4 isoforms of apolipoprotein E. -. ... immunogen = human apolipoprotein E. reacts to the E2, E3 and E4 isoforms of apolipoprotein E. -. ... reacts to the E2, E3 and E4 isoforms of apolipoprotein E. -. Apo E (IB5-E1). Acris Antibodies. monoclonal. IgG1. Mouse. ( ... immunogen = human Apolipoprotein E. detects all three common isoforms of ApoE (E2, E3, E4). -. ...
Apolipoprotein E2 / genetics * Apolipoprotein E2 / metabolism * Chronic Disease * Dental Amalgam / adverse effects ... A significant correlation was found between CMT and the Apo-lipoprotein E4 genotype (p=0.001). An investigation into an ...
Statement on use of apolipoprotein E testing for Alzheimer disease. JAMA. 1995;274:1627-1629. ... Apoliprotein E-E3 or E2) and the association with other diseases (e.g., coronary heart disease). ... such as Apolipoprotein E-E4) associated with variable disease risks. In the case of genes associated with multiple disease ... Apolipoprotein E-E4 allele and Alzheimers disease). Authors should acknowledge the presence of other gene variants (e.g., ...
Mouse Monoclonal Anti-Apolipoprotein M/ApoM Antibody (8F12C6B8) [Alexa Fluor® 488]. Validated: WB, ELISA, ICC/IF. Tested ... Additional Apolipoprotein M/ApoM Products. Apolipoprotein M/ApoM NB110-60526AF488 * Apolipoprotein M/ApoM Antibodies ... Home » Apolipoprotein M/ApoM » Apolipoprotein M/ApoM Antibodies » Apolipoprotein M/ApoM Antibody (8F12C6B8) [Alexa Fluor® 488] ... Blogs on Apolipoprotein M/ApoM. There are no specific blogs for Apolipoprotein M/ApoM, but you can read our latest blog posts. ...
Apolipoprotein A-IV/ApoA4 Antibody Pair. Matched antibody pairs validated for ELISA or IP-Western Blot. Backed by our 100% ... Additional Apolipoprotein A-IV/ApoA4 Products. Apolipoprotein A-IV/ApoA4 H00000337-AP21 * Apolipoprotein A-IV/ApoA4 Antibodies ... Home » Apolipoprotein A-IV/ApoA4 » Apolipoprotein A-IV/ApoA4 Antibody Pairs » Apolipoprotein A-IV/ApoA4 Antibody Pair ... Blogs on Apolipoprotein A-IV/ApoA4. There are no specific blogs for Apolipoprotein A-IV/ApoA4, but you can read our latest blog ...
APOE alleles (e2, e3, e4) were determined using PCR. Comparisons of allele frequencies between groups were made. RESULTS: There ... Apolipoprotein E4 / genetics*. Child, Preschool. Female. Gene Frequency. Genetic Predisposition to Disease. Humans. Infant. ...
There are three homozygous phenotype including: Apo E2, ApoE3 and ApoE4 alleles present in men27,28,29. The Apo E2 and E4 ... Apolipoprotein E regulates dietary cholesterol absorption and biliary cholesterol excretion: studies in C57BL/6 apolipoprotein ... Apolipoprotein E: far more than a lipid transport protein. Annu Rev Genomics Hum Genet 1, 507-537 (2000). ... Apolipoprotein E deficiency leads to cutaneous foam cell formation in mice. J Invest Dermatol 104, 246-250 (1995). ...
The apolipoprotein B (apoB) 5′ UTR cis regulatory element is an RNA element located in the 5′ UTR of the human apoB mRNA. This ... Page for Apolipoprotein B (apoB) 5′ UTR cis-regulatory element at Rfam v t e. ... Pontrelli L, Sidiropoulos KG, Adeli K (June 2004). "Translational control of apolipoprotein B mRNA: regulation via cis elements ...
  • Aims: Genetic variation at the apolipoprotein E (apoE) locus is an important determinant of plasma lipids. (ebscohost.com)
  • Although the importance of human apolipoprotein E (apoE) in vascular diseases has clearly been established, most of the research on apoE has focused on its role in cholesterol metabolism. (ebscohost.com)
  • Background: Apolipoprotein E (APOE) polymorphism is associated with lipid levels. (ebscohost.com)
  • Corbo RM, Scacchi R. Apolipoprotein E (APOE) allele distribution in the world. (medscape.com)
  • We studied the relationship of apolipoprotein E (apoE) isoforms and coronary artery disease (CAD) in 224 African Americans and 326 Caucasians undergoing diagnostic coronary angiography. (elsevier.com)
  • The apolipoprotein E (apoE) is a classic example of a gene exhibiting pleiotropism. (cdc.gov)
  • Human apolipoprotein (ApoE) genotype influences the development of Alzheimer's disease and cerebral amyloid angiopathy (CAA), where the ε4 allele increases and the ε2 allele decreases the risk for developing disease. (duke.edu)
  • Apolipoprotein E (ApoE) and its isoforms (e2, e3, and e4) are involved in the regulation of lipid metabolism. (hindawi.com)
  • Specifically, ApoE e4 has been associated with atherosclerotic diseases, while e2 has a favorable effect. (hindawi.com)
  • Apolipoprotein E (ApoE) is an important circulating serum protein involved in transporting lipids and cholesterol and regulating lipid levels. (hindawi.com)
  • APOE alleles (e2, e3, e4) were determined using PCR. (biomedsearch.com)
  • Apolipoprotein E ( ApoE ) is a class of proteins involved in the metabolism of fats in the body. (wikidoc.org)
  • The gene, APOE , is mapped to chromosome 19 in a cluster with apolipoprotein C1 (APOC-I) and the apolipoprotein C2 . (wikidoc.org)
  • 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. (jneurosci.org)
  • Apolipoprotein E (apoE) is a protein ( M r = 35,000) that functions in the CNS. (jneurosci.org)
  • The aim of this study was to evaluate whether treatment with the ACE inhibitor perindopril affects diabetes-induced plaque formation in the apolipoprotein E (apoE)-deficient mouse. (ahajournals.org)
  • Apolipoprotein E (apoE) is an important transporter of fats in the blood. (clinicaltrials.gov)
  • ApoE comes in E2, E3 and E4 forms, depending on your genetic make up. (clinicaltrials.gov)
  • Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. (dovepress.com)
  • The apolipoprotein E (APOE) gene is located on chromosome 19 and encodes a glycoprotein that is 299 amino acids long. (dovepress.com)
  • Several major APOE isoforms can be distinguished: E2, E3, and E4. (dovepress.com)
  • The 4 allele of the apolipoprotein E (APOE) gene is known as a risk factor for cognitive impairment. (dovepress.com)
  • Apolipoprotein E deficient mice (ApoE-/-), a mouse model of atherosclerosis, and their wild-type (WT) counterparts were used to assess agonist-stimulated synthesis of prostacyclin (PGI 2 ), inhibition of platelet aggregation ex vivo, and intra-platelet cAMP levels. (nih.gov)
  • Six possible apoE genotypes exist: e2/e2, e2/e3, e2/e4, e3/e3, e3/e4 and e4/e4. (medindia.net)
  • Objective- Apolipoprotein E (apoE) and apolipoprotein B100 (apoB) are both involved in receptor-mediated uptake of atherogenic lipoproteins by the liver. (ahajournals.org)
  • Apolipoprotein E (apoE) and apolipoprotein B100 (apoB) are synthesized in the liver and other organs. (ahajournals.org)
  • Genetic testing for late-onset Alzheimer's involves one gene, the apolipoprotein E ( APOE ) gene on the 19th chromosome. (medpagetoday.com)
  • Two major genotypes are known to affect the development and progression of Alzheimer's disease (AD) and its response to cholinesterase inhibitors: the apolipoprotein E (ApoE) and butyrylcholinesterase genes (BChE). (ebscohost.com)
  • The ε4 allele of the apolipoprotein E gene (APOE) is a major risk factor for late-onset Alzheimer's disease (LOAD) but is neither necessary nor sufficient to cause the disease. (ebscohost.com)
  • To investigate the possible involvement of the butyrylcholinesterase (BCHE) K variant and transferrin (TF) C2 variant in the manifestation of Alzheimer's disease (AD), we analyzed the BCHE, TF and apolipoprotein E (APOE) genotypes of 164 sporadic AD patients and 239 normal elderly. (ebscohost.com)
  • In a consecutive hospital-based autopsy series, we examined the relationship between apolipoprotein E (apoE) and Alzheimer's disease (AD) and investigated the clinicopathological relationship in AD. (ebscohost.com)
  • Several lines of evidence indicate that apolipoprotein E (apoE) plays a central role in the brain's response to injury and neurodegeneration in the adult. (ebscohost.com)
  • The APOE É›4 allele modulates brain white matter integrity in healthy adults. (ebscohost.com)
  • The Apolipoprotein E (APOE) É›4 allele is the best-established genetic risk factor for sporadic Alzheimer's disease, and is also associated with structural gray matter and functional brain changes in healthy young, middle-aged and elderly subjects. (ebscohost.com)
  • The presence of apolipoprotein E4 ( APOE * E4 ) is the strongest currently known genetic risk factor for Alzheimer disease and is associated with brain gray matter loss, notably in areas involved in Alzheimer disease pathology. (ajnr.org)
  • the rare APOE e2 allele has the opposite effect. (medpagetoday.com)
  • The binding of the remnants to hepatic lipoprotein receptors is mediated by apolipoprotein E (apoE). (renalandurologynews.com)
  • Recent excitement has centered around the discovery of the relationship between the apolipoprotein E (apoE) gene and Alzheimer s Disease. (ec-online.net)
  • In about 10% of the cases, FD is caused by autosomal dominant mutations in the apolipoprotein E gene (APOE). (bireme.br)
  • Dr. Thompson will investigate the brain changes at work with the apolipoprotein E (APOE) gene variation known as APOE-e2, which provides protection against developing Alzheimer's. (alz.org)
  • Dr. Thompson and colleagues will launch the ENIGMA-APOE-e2 initiative, a brain aging study across 35 countries to study the protective effects of the genetic variation in diverse populations worldwide. (alz.org)
  • The researchers will measure brain volume and brain electrical activity from more than 30,000 participants worldwide in the ongoing ENIGMA Consortium study who have the APOE-e2 genetic variation. (alz.org)
  • The gene encoding ApoE is polymorphic - meaning it has multiple alleles - which translates to three protein isoforms: E2, E3, and E4. (taconic.com)
  • Sleep Apnea May Increase the Risk of Dementia in Older Men Without the Apolipoprotein E (APOE) ε4 Allele: Some 7547 men without dementia or other active neurological conditions that affect cognition were interviewed at baseline for sleep apnea. (psychiatrictimes.com)
  • The effect of self-reported sleep apnea on dementia risk depended on their APOE É 4 status. (psychiatrictimes.com)
  • whereas there was no additional risk for participants with the APOE É 4 allele. (psychiatrictimes.com)
  • Apolipoprotein E antibody LS-C533481 is an FITC-conjugated goat polyclonal antibody to human Apolipoprotein E (APOE). (lsbio.com)
  • Carriers of either the e2 or e4 allele of the apolipoprotein E (APOE) gene have an elevated risk of intracerebral hemorrhage. (thefreedictionary.com)
  • Apolipoprotein E. Apolipoprotein E (APOE) is a class of apolipoprotein found in the chylomicron and Intermediate-density lipoprotein (IDLs) that is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. (pearltrees.com)
  • Apolipoprotein (apo) E isoforms are key determinants of susceptibility to Alzheimer's disease. (jneurosci.org)
  • There are several allelic isoforms (such as E2, E3, and E4). (harvard.edu)
  • Recognizes human Apolipoprotein E (Apo E). Recognizes isoforms E2, E3 and E4. (lsbio.com)
  • The aim of the present study was to evaluate the association between apolipoprotein E genotype and plasma lipid levels among a rural black population in South Africa. (ebscohost.com)
  • Associations between Apolipoprotein E Genotype, Diet, Body Mass Index, and Serum Lipids in Lithuanian Adult Population. (ebscohost.com)
  • She was diagnosed with partial lipoprotein lipase (LPL) deficiency but without an associated LPL gene mutation in the presence of the apolipoprotein E3/2 genotype. (kjim.org)
  • This is the first reported case of extreme gestational hyperlipidemia with a partial LPL deficiency in the absence of an LPL gene mutation and the apolipoprotein E 3/2 genotype. (kjim.org)
  • The effect of partial LPL deficiency and dysbetalipoproteinemia can be modulated by other genes, such as apolipoprotein (apo) E. Apo E2 has a lower binding affinity to the hepatic receptor [ 3 , 4 ], and patients with the apo E3/2 genotype are associated with higher plasma lipid levels compared to those without the apo E2 allele [ 5 , 6 ]. (kjim.org)
  • Apolipoprotein E genotype and outcome after aneurysmal subarachnoid hemorrhage. (biomedsearch.com)
  • The isoform e3e3 is more common among Pakistani population and genotype E2 can be considered as lipid lowering and protective. (thefreedictionary.com)
  • Apolipoprotein E genotype and the association between C-reactive protein and postoperative delirium: Importance of gene-protein interactions. (harvard.edu)
  • The common apolipoprotein E alleles (ε4, ε3, and ε2) are important genetic risk factors for late-onset Alzheimer's disease, with the ε4 allele increasing risk and reducing the age of onset and the ε2 allele decreasing risk and markedly delaying the age of onset. (duke.edu)
  • The apolipoprotein E gene comes in three different forms, known as alleles. (ukbiobank.ac.uk)
  • These alleles are called e2, e3 and e4. (ukbiobank.ac.uk)
  • 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. (bmj.com)
  • Frequencies of the e2, e3, and e4 alleles in gout were 0.061, 0.817 and 0.122, compared with the corresponding control frequencies of 0.057, 0.858 and 0.085. (bmj.com)
  • Intracerebral adeno-associated virus gene delivery of apolipoprotein E2 markedly reduces brain amyloid pathology in Alzheimer's disease mouse models. (duke.edu)
  • Verghese, P. B., Castellano, J. M. & Holtzman, D. M. Apolipoprotein E in Alzheimer's disease and other neurological disorders. (nature.com)
  • For example, issues are currently debated regarding population-based genetic testing for breast cancer in relation to BRCA1 (5), Alzheimer's disease in relation to the Apolipoprotein E-E4 allele (6), and iron overload in relation to the hemochromatosis gene (7). (cdc.gov)
  • Amsterdam, The Netherlands and Sun City, AZ, USA, January 15, 2009 Researchers at Banner Health's Sun Health Research Institute have uncovered evidence that Alzheimer's disease (AD) may be clinically confirmed in patients with apolipoprotein E2 homozygote. (bio-medicine.org)
  • Clinical confirmation of the apolipoprotein E2 homozygote Alzheimer's disease finding in this study was confirmed by MRI, PET and neuropsychological evaluation and testing. (bio-medicine.org)
  • Apolipoprotein E allelotype is associated with neuropathological findings in Alzheimer's disease. (ebscohost.com)
  • To determine the association between the e4 allele of apolipoprotein E and Alzheimer's disease in a randomly selected population sample. (bmj.com)
  • Allele e4 of apolipoprotein is associated with Alzheimer's disease in a dose-response fashion in a randomly selected elderly population. (bmj.com)
  • RF 1-2* Evidence is accumulating that apolipoprotein E is important in late onset Alzheimer's disease. (bmj.com)
  • The first evidence that e4 allele of apolipoprotein E could be associated with Alzheimer's disease was published by Pericak-Vance et al. (bmj.com)
  • All the studies that have investigated the relation between apolipoprotein E polymorphism and Alzheimer's disease have included highly selected patients and corresponding controls. (bmj.com)
  • Bathing the mouse brain in the APOE2 form of apolipoprotein E reduced levels of abnormal beta-amyloid protein compared with controls, suggesting that the protein could prevent Alzheimer's disease, researchers said. (medpagetoday.com)
  • The article is " Possible Alzheimer's Disease in an Apolipoprotein E2 Homozygote " by Ignat Ignatov, Christine Belden, Sandra Jacobson, Donald Connor and Marwan N. Sabbagh. (j-alz.com)
  • Apolipoprotein E genotypes and their relation to lipid levels in a rural South African population. (ebscohost.com)
  • Cardiovascular Risk According to Plasma Apolipoprotein and Lipid Profiles in a Canadian First Nation**This article is part of a joint publication initiative between Preventing Chronic Disease and Chronic Diseases in Canada. (cdc.gov)
  • [9] [10] Two viral envelope glycoproteins , E1 and E2 , are embedded in the lipid envelope. (wikipedia.org)
  • 27-29 The concentrations of these particles have been evaluated with a number of different methods based on their density, size, charge, specific lipid components, apolipoprotein composition, or immunoaffinity. (ahajournals.org)
  • While LDL, HDL, and (sometimes) VLDL (very low-density lipoprotein) are the only classes mentioned in regards to diagnostic tests, there are four other classes of lipoproteins that differ in size, lipid composition, and apolipoproteins. (taconic.com)
  • Apolipoproteins are protein-lipid complexes that bind oil-soluble substances such as fat and cholesterol. (taconic.com)
  • Weinberg RB, Spector MS (1985) Structural properties and lipid binding of human apolipoprotein AIV. (springer.com)
  • T (rs2075291) in apolipoprotein A5 gene to determination of triglycerides levels in CAD patients receiving, atorvastatin, lipid lowering drug. (springer.com)
  • In both male and female mice, E2 increased calcified area in a site-specific manner in the aortic sinus independently of plaque growth or lipid levels and occurred in association with a site-specific decrease in the proportion of ERβ-positive intimal cells. (ovid.com)
  • OBJECTIVE--To elucidate the relationship, if any, between lipid abnormalities and apolipoprotein E (apo E) polymorphism, by investigating apo E phenotype and allele frequency. (bmj.com)
  • The goal of this review is to provide an overview of the involvement of Aβ, tau and apolipoprotein E4 (apoE4), the major genetic risk factor in late-onset AD (LOAD), in GABAergic neurotransmission and the potential of modulating the GABAergic function as AD therapy. (frontiersin.org)
  • Davignon J, Gregg RE, Sing CF. Apolipoprotein E polymorphism and atherosclerosis. (medscape.com)
  • [16] E2 is associated with both increased and decreased risk for atherosclerosis . (wikidoc.org)
  • Methods and Results- In a postmortem study involving 49 patients (22 patients with symptomatic atherosclerosis), we quantified apolipoprotein deposits in arterial rings obtained from the left main coronary, the common carotid, the common iliac, and the renal artery applying tissue microarray technology and semiquantitative immunohistochemistry. (ahajournals.org)
  • Conclusions- Increased apolipoprotein deposits are an early sign of symptomatic atherosclerosis. (ahajournals.org)
  • Avogaro P, Bittolo-Bon G, Cazzolato G, Quinci GB (1979) Are apolipoproteins better discriminators than lipids for atherosclerosis? (springer.com)
  • Apolipoprotein D (Apo-D) is a component of high-density lipoprotein that has no marked similarity to other apolipoprotein sequences. (wikipedia.org)
  • 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. (springer.com)
  • Apolipoprotein E is a fat-binding protein ( apolipoprotein ) that is part of the chylomicron and intermediate-density lipoprotein (IDLs) . (wikidoc.org)
  • VLDL that possess apoB-100 as their major structural protein but equally key functional apolipoproteins such as apoC-I, apoC-II, and apoC-III are remodeled similarly in circulation through hydrolysis by enzyme lipoprotein lipase (LPL), which results in reduction of size with generation of remnant particles. (ahajournals.org)
  • Association of Apolipoprotein E in Lipoprotein Subspecies With Risk of Dementia. (harvard.edu)
  • 4-6 The apolipoproteins are the protein part of the lipoprotein particles and play an important role in the interaction of lipoproteins with cells and the extracellular matrix. (ahajournals.org)
  • 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. (tudelft.nl)
  • Plasma apolipoprotein E phenotypes modulate lipoprotein concentrations, particularly that of low density lipoprotein cholesterol. (bmj.com)
  • In particular, increased apolipoprotein B levels, both in whole plasma and in specific lipoprotein fractions, e.g. low density lipoproteins (LDL) [3], seem to be associated to a raised risk, the opposite being the case for apo AI [4]. (springer.com)
  • Mahley RW, Rall SC Jr. Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal metabolism. (medscape.com)
  • It is hypothesized that apolipoprotein E (Apo E), which is involved in cholesterol metabolism, might play a role in this process. (medscimonit.com)
  • Fidge NH (1980) The redistribution and metabolism of iodinated apolipoprotein AIV in rats. (springer.com)
  • OBJECTIVE -Dysregulated apolipoprotein (apo)C-III metabolism may account for hypertriglyceridemia and increased cardiovascular risk in the metabolic syndrome. (diabetesjournals.org)
  • Apolipoprotein D is a protein that in humans is encoded by the APOD gene. (wikipedia.org)
  • Apolipoprotein (apo) E is a 34 kDa protein that participates in the transport of plasma lipids and in the redistribution of lipids among cells ( Mahley, 1988 ). (jneurosci.org)
  • Human apolipoprotein E2 promotes parenchymal amyloid deposition and neuronal loss in vasculotropic mutant amyloid-β protein Tg-SwDI mice. (duke.edu)
  • The proteins of this virus are arranged along the genome in the following order: N terminal-core-envelope (E1)-E2-p7-nonstructural protein 2 (NS2)-NS3-NS4A-NS4B-NS5A-NS5B-C terminal. (wikipedia.org)
  • Negative-stain electron microscopy revealed that the particles were spherical (~40- to 75-nm diameter) and pleomorphic and that some of them contain HCV E2 protein and apolipoprotein E on their surfaces. (pubmedcentralcanada.ca)
  • In vitro, E2 suppressed ERβ expression and increased VSMC mineralization, demonstrating increased collagen I and II, osteocalcin and bone sialoprotein, and reduced matrix Gla protein and osteopontin. (ovid.com)
  • Unlike other lipoproteins, which are mainly produced in the liver, apolipoprotein D is mainly produced in the brain and testes. (wikipedia.org)
  • They may reflect either enhanced retention of atherogenic lipoproteins or impaired local apolipoprotein degradation. (ahajournals.org)
  • Swaney JB, Braithwaite F, Eder HA (1977) Characterization of the apolipoproteins of rat plasma lipoproteins. (springer.com)
  • Brewer HB, Fairwell T, La Rue A, Rorian R, Hauser A, Bronzert TJ (1978) The amino acid sequence of human apo AI, an apolipoprotein isolated from high density lipoproteins. (springer.com)
  • Noma A Yokosuka T, Kitamura K (1983) Plasma lipids and apolipoproteins as discriminators for presence and severity of angiographically defined coronary artery disease. (springer.com)
  • 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. (springer.com)
  • This usually occurs in the setting of an abnormal apolipoprotein-E isoform, apo-E2. (oncologynurseadvisor.com)
  • When the apo-E2 isoform is present there is impaired uptake of chylomicron and VLDL remnants by the liver. (oncologynurseadvisor.com)
  • Homozygous apo E2 may result in type III Hyperlipidaemia. (edu.au)
  • Type III hyperlipoproteinemia (HLP) is mainly found in homozygous apolipoprotein (APO) E2 (R158C) carriers. (tudelft.nl)
  • Interestingly, the homozygous apolipoprotien-E2 state occurs more commonly in the population (1/100 persons) than the clinical syndrome of familial dysbetalipoproteinemia (1/10,000 persons). (oncologynurseadvisor.com)
  • Here, our aim was to examine whether VLDL and apolipoprotein (apo) CIII induce endoplasmic reticulum (ER) stress, inflammation and insulin resistance in skeletal muscle. (springer.com)
  • 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. (tudelft.nl)
  • Apolipoprotein E2 (apoE2)-associated hyperlipidemia is characterized by a disturbed clearance of apoE2-enriched VLDL remnants. (tudelft.nl)
  • RESULTS: Apolipoprotein E epsilon2 or epsilon4-containing genotypes were not associated with outcome, occurrence of cerebral infarction, or with any of their predictors, either in univariate or multivariate analysis. (biomedsearch.com)
  • The apolipoprotein B (apoB) 5′ UTR cis regulatory element is an RNA element located in the 5′ UTR of the human apoB mRNA. (wikipedia.org)
  • The assessment of plasma TG concentration as an independent predictor for CAD is complicated by the fact that (1) there is considerable interindividual and intraindividual variation in plasma TG levels and (2) circulating TRL are highly heterogeneous in size, density, and composition and may consist of intestinally derived apolipoprotein (apo) B-48-containing chylomicrons and chylomicron remnants, in addition to liver-derived apoB-100-containing VLDL and their remnants. (ahajournals.org)
  • In addition to apolipoprotein (apo)E, HCV particles also incorporate apoB and apoA-I. In general, host apolipoproteins were more readily accessible to antibody labeling than HCV glycoproteins, suggesting either lower abundance or masking by host proteins. (pnas.org)
  • There are currently no images for Apolipoprotein M/ApoM Antibody (NB110-60526AF488). (novusbio.com)
  • Sandwich ELISA: Apolipoprotein A-IV/ApoA4 Antibody Pair [H00000337-AP21] - Detection sensitivity ranging from 0.3 ng/ml to 100 ng/ml. (novusbio.com)
  • There are no publications for Apolipoprotein A-IV/ApoA4 Antibody Pair (H00000337-AP21). (novusbio.com)
  • E1 and E2 are covalently bonded when embedded in the envelope of HCV and are stabilized by disulfide bonds . (wikipedia.org)
  • Zhang SH, Reddick RL, Piedrahita JA, Maeda N. Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science . (medscape.com)
  • Inhibition of platelet aggregation ex vivo is repressed in apolipoprotein E deficient mice. (nih.gov)
  • The objective of this work was to examine the ability of 17β-estradiol (E2) to stimulate calcification of vascular smooth muscle cells (VSMC) in vivo, using aged apolipoprotein E-null mice with advanced atherosclerotic lesions, and subsequently to explore underlying mechanisms in vitro. (ovid.com)
  • Silastic E2 capsules were implanted into male and female apolipoprotein E-null mice aged 34 weeks. (ovid.com)
  • Apolipoprotein E2 homozygote has been associated with a protective eff. (bio-medicine.org)
  • Apolipoprotein E2 homozygote has been associated with a protective effect against AD and contributes to delaying the onset of symptoms. (bio-medicine.org)
  • However previously, no significant data had pointed to clinically confirmed AD in persons with apolipoprotein E2 homozygote. (bio-medicine.org)
  • Apolipoprotein E phenotypes in patients with gout: relation with hypertriglyceridaemia. (bmj.com)
  • Protective role of the apolipoprotein E2 allele in age-related disease traits and survival: evidence from the Long Life Family Study. (cdc.gov)
  • The E1, E2, and core structural proteins are required for particle formation ( 5 , 6 ) but not for viral RNA replication or translation ( 7 , 40 ). (pubmedcentralcanada.ca)
  • Individuals with an E2/E2 combination may clear dietary fat slowly and be at greater risk for early vascular disease and the genetic disorder type III hyperlipoproteinemia -94.4% of such patients are E2/E2, while only ∼2% of E2/E2 develop the disease, so other environmental and genetic factors are likely to be involved (such as cholesterol in the diet and age). (wikidoc.org)
  • These complex molecules have a "shell" composed of cholesterol, phospholipids, and apolipoproteins, and a core with the transport material: cholesterol esters and triglycerides (see Figure 1). (taconic.com)
  • Chen CH, Albers JJ (1985) Activation of lecithin:cholesterol acyltransferase by apolipoproteins E-2, E-3, and AIV isolated from human plasma. (springer.com)
  • A hypervariable region , the hypervariable region 1 (HVR1) can be found on the E2 glycoprotein. (wikipedia.org)
  • In this report, we generated an infectious HCV genome with an affinity tag fused to the E2 envelope glycoprotein. (pnas.org)
  • Apolipoprotein (apo)-C-III is an 8.8-kDa glycoprotein synthesized by the liver and intestines. (diabetesjournals.org)
  • Apolipoproteins E" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
  • Smelt AH, de Beer F. Apolipoprotein E and familial dysbetalipoproteinemia: clinical, biochemical, and genetic aspects. (medscape.com)
  • 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. (springer.com)
  • 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. (springer.com)
  • We have demonstrated that E2 can drive calcification in advanced atherosclerotic lesions by promoting the differentiation of VSMC to osteoblast-like cells, a process which is augmented by inhibition of estrogen receptor alpha or ERβ activity. (ovid.com)
  • Previous studies have confirmed that apolipoprotein E4 is a predictive risk factor for AD and indicates an increased genetic risk of AD. (bio-medicine.org)
  • 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]. (springer.com)
  • 13 In the present analysis, we used the tissue microarrays to investigate the pattern and extent of apolipoprotein deposits in the arterial wall of vulnerable patients and compared these findings with asymptomatic patients who did not develop cardiovascular events during their lifetime. (ahajournals.org)
  • The results of 3 new studies in geriatric psychiatry show that mentally stimulating activities may decrease the risk of mild cognitive impairment, targeted noninvasive brain stimulation may combat specific memory impairments, and sleep apnea may increase the risk of dementia in older men without the apolipoprotein E ε4 allele. (psychiatrictimes.com)
  • The aim of the study was to evaluate a possible effect of atorvastatin on renal interleukins (ILs) and prostaglandin E2 (PGE2) in type 1 diabetic rats. (springer.com)
  • Among them, prostaglandin E2 (PGE2) enhances aggregation of platelets submaximally stimulated in vitro. (rupress.org)
  • Approximately 60% of the UK population are E3/E3, 25% E4 carriers and 15% E2 carriers. (clinicaltrials.gov)
  • The diagnosis of dysbetalipoproteinemia can be confirmed by the identification of the mutant apolipoprotien-E2 allele. (oncologynurseadvisor.com)
  • Therefore, Apo E2 might interact with other disease-related factors to accelerate the onset of CAD in some patients with SLE and as such might be an additional marker of risk in this population. (medscimonit.com)
  • Among the symptomatic patients, those without diabetes had more intense apolipoprotein deposits than diabetics. (ahajournals.org)
  • High-Glucose-Induced Endothelial Cell Injury Is Inhibited by a Peptide Derived from Human Apolipoprotein E. Bhattacharjee, Partha S. (ebscohost.com)