Apolipoproteins E: A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.Apolipoprotein E4: A major and the second most common isoform of apolipoprotein E. In humans, Apo E4 differs from APOLIPOPROTEIN E3 at only one residue 112 (cysteine is replaced by arginine), and exhibits a lower resistance to denaturation and greater propensity to form folded intermediates. Apo E4 is a risk factor for ALZHEIMER DISEASE and CARDIOVASCULAR DISEASES.Apolipoprotein E3: A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.Apolipoprotein E2: One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.Apolipoprotein A-I: The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.Apolipoprotein B-100: A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.Apolipoproteins B: Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.Apolipoproteins: Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.Apolipoprotein C-III: A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).Apolipoprotein C-I: A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.Apolipoprotein A-II: The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.Apolipoprotein C-II: A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.Apolipoproteins A: Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.Apolipoprotein B-48: A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Apolipoproteins C: A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.Lipoproteins, VLDL: A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.Lipoproteins: Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.Lipoproteins, HDL: A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.Receptors, LDL: Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.Alzheimer Disease: A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)Hyperlipoproteinemia Type III: An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.TriglyceridesGenotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Lipids: A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Alleles: Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.Arteriosclerosis: Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Apoprotein(a): A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.Lipoproteins, LDL: A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.Hyperlipoproteinemias: Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.Receptors, Lipoprotein: Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.Polymorphism, Genetic: The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.Mice, Inbred C57BLLipoprotein(a): A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.LDL-Receptor Related Proteins: A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).Apolipoproteins D: A glycoprotein component of HIGH-DENSITY LIPOPROTEINS that transports small hydrophobic ligands including CHOLESTEROL and STEROLS. It occurs in the macromolecular complex with LECITHIN CHOLESTEROL ACYLTRANSFERASE. Apo D is expressed in and secreted from a variety of tissues such as liver, placenta, brain tissue and others.Cholesterol, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.Low Density Lipoprotein Receptor-Related Protein-1: A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Hyperlipidemias: Conditions with excess LIPIDS in the blood.Amyloid beta-Peptides: Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.Cholesterol, LDL: Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.Lipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.ATP Binding Cassette Transporter 1: A superfamily of large integral ATP-binding cassette membrane proteins whose expression pattern is consistent with a role in lipid (cholesterol) efflux. It is implicated in TANGIER DISEASE characterized by accumulation of cholesteryl ester in various tissues.Gene Frequency: The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.Aorta: The main trunk of the systemic arteries.Chylomicrons: A class of lipoproteins that carry dietary CHOLESTEROL and TRIGLYCERIDES from the SMALL INTESTINE to the tissues. Their density (0.93-1.006 g/ml) is the same as that of VERY-LOW-DENSITY LIPOPROTEINS.Diet, Atherogenic: A diet that contributes to the development and acceleration of ATHEROGENESIS.Hypercholesterolemia: A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Lipoprotein Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.Cholesterol, VLDL: Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.Heterozygote: An individual having different alleles at one or more loci regarding a specific character.Phosphatidylcholine-Sterol O-Acyltransferase: An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Isoelectric Focusing: Electrophoresis in which a pH gradient is established in a gel medium and proteins migrate until they reach the site (or focus) at which the pH is equal to their isoelectric point.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Hyperlipoproteinemia Type II: A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).Macrophages: The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)Hypertriglyceridemia: A condition of elevated levels of TRIGLYCERIDES in the blood.Lipoproteins, IDL: A mixture of very-low-density lipoproteins (VLDL), particularly the triglyceride-poor VLDL, with slow diffuse electrophoretic mobilities in the beta and alpha2 regions which are similar to that of beta-lipoproteins (LDL) or alpha-lipoproteins (HDL). They can be intermediate (remnant) lipoproteins in the de-lipidation process, or remnants of mutant CHYLOMICRONS and VERY-LOW-DENSITY LIPOPROTEINS which cannot be metabolized completely as seen in FAMILIAL DYSBETALIPOPROTEINEMIA.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Hypolipoproteinemias: Conditions with abnormally low levels of LIPOPROTEINS in the blood. This may involve any of the lipoprotein subclasses, including ALPHA-LIPOPROTEINS (high-density lipoproteins); BETA-LIPOPROTEINS (low-density lipoproteins); and PREBETA-LIPOPROTEINS (very-low-density lipoproteins).Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Homozygote: An individual in which both alleles at a given locus are identical.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Aortic Diseases: Pathological processes involving any part of the AORTA.Brain: The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Cholesterol, Dietary: Cholesterol present in food, especially in animal products.Foam Cells: Lipid-laden macrophages originating from monocytes or from smooth muscle cells.Clusterin: A highly conserved heterodimeric glycoprotein that is differentially expressed during many severe physiological disturbance states such as CANCER; APOPTOSIS; and various NEUROLOGICAL DISORDERS. Clusterin is ubiquitously expressed and appears to function as a secreted MOLECULAR CHAPERONE.Dimyristoylphosphatidylcholine: A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.Hyperlipoproteinemia Type V: A severe type of hyperlipidemia, sometimes familial, that is characterized by the elevation of both plasma CHYLOMICRONS and TRIGLYCERIDES contained in VERY-LOW-DENSITY LIPOPROTEINS. Type V hyperlipoproteinemia is often associated with DIABETES MELLITUS and is not caused by reduced LIPOPROTEIN LIPASE activity as in HYPERLIPOPROTEINEMIA TYPE I .Protein Isoforms: Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.Risk Factors: An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.Cerebral Amyloid Angiopathy: A heterogeneous group of sporadic or familial disorders characterized by AMYLOID deposits in the walls of small and medium sized blood vessels of CEREBRAL CORTEX and MENINGES. Clinical features include multiple, small lobar CEREBRAL HEMORRHAGE; cerebral ischemia (BRAIN ISCHEMIA); and CEREBRAL INFARCTION. Cerebral amyloid angiopathy is unrelated to generalized AMYLOIDOSIS. Amyloidogenic peptides in this condition are nearly always the same ones found in ALZHEIMER DISEASE. (from Kumar: Robbins and Cotran: Pathologic Basis of Disease, 7th ed., 2005)Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Hyperlipoproteinemia Type IV: A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits.ATP-Binding Cassette Transporters: A family of MEMBRANE TRANSPORT PROTEINS that require ATP hydrolysis for the transport of substrates across membranes. The protein family derives its name from the ATP-binding domain found on the protein.Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Hypobetalipoproteinemias: Conditions with abnormally low levels of BETA-LIPOPROTEINS (low density lipoproteins or LDL) in the blood. It is defined as LDL values equal to or less than the 5th percentile for the population. They include the autosomal dominant form involving mutation of the APOLIPOPROTEINS B gene, and the autosomal recessive form involving mutation of the microsomal triglyceride transfer protein. All are characterized by low LDL and dietary fat malabsorption.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Brachiocephalic Trunk: The first and largest artery branching from the aortic arch. It distributes blood to the right side of the head and neck and to the right arm.Kinetics: The rate dynamics in chemical or physical systems.Cognition Disorders: Disturbances in mental processes related to learning, thinking, reasoning, and judgment.Plaque, Atherosclerotic: Lesions formed within the walls of ARTERIES.Cholesterol Ester Transfer Proteins: Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.Dementia: 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.Plaque, Amyloid: Accumulations of extracellularly deposited AMYLOID FIBRILS within tissues.Age of Onset: 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.Lipoproteins, HDL3: Intermediate-density subclass of the high-density lipoproteins, with particle sizes between 7 to 8 nm. As the larger lighter HDL2 lipoprotein, HDL3 lipoprotein is lipid-rich.Reference Values: The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.Neurofibrillary Tangles: 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.Scavenger Receptors, Class B: A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.Amyloid beta-Protein Precursor: 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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Kringles: Triple-looped protein domains linked by disulfide bonds. These common structural domains, so-named for their resemblance to Danish pastries known as kringlers, play a role in binding membranes, proteins, and phospholipids as well as in regulating proteolysis. Kringles are also present in coagulation-related and fibrinolytic proteins and other plasma proteinases.Neuropsychological Tests: 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.Aging: The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.Time Factors: Elements of limited time intervals, contributing to particular results or situations.DNA: A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).Particle Size: Relating to the size of solids.Ultracentrifugation: Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.Sinus of Valsalva: The dilatation of the aortic wall behind each of the cusps of the aortic valve.Tangier Disease: An autosomal recessively inherited disorder caused by mutation of ATP-BINDING CASSETTE TRANSPORTERS involved in cellular cholesterol removal (reverse-cholesterol transport). It is characterized by near absence of ALPHA-LIPOPROTEINS (high-density lipoproteins) in blood. The massive tissue deposition of cholesterol esters results in HEPATOMEGALY; SPLENOMEGALY; RETINITIS PIGMENTOSA; large orange tonsils; and often sensory POLYNEUROPATHY. The disorder was first found among inhabitants of Tangier Island in the Chesapeake Bay, MD.Genetic Variation: Genotypic differences observed among individuals in a population.Hyperlipidemia, Familial Combined: A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.Dementia, Vascular: 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)Recombinant Proteins: Proteins prepared by recombinant DNA technology.Serum Amyloid A Protein: An ACUTE PHASE REACTION protein present in low concentrations in normal sera, but found at higher concentrations in sera of older persons and in patients with AMYLOIDOSIS. It is the circulating precusor of amyloid A protein, which is found deposited in AA type AMYLOID FIBRILS.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Polymorphism, Restriction Fragment Length: Variation occurring within a species in the presence or length of DNA fragment generated by a specific endonuclease at a specific site in the genome. Such variations are generated by mutations that create or abolish recognition sites for these enzymes or change the length of the fragment.Receptors, Scavenger: A large group of structurally diverse cell surface receptors that mediate endocytic uptake of modified LIPOPROTEINS. Scavenger receptors are expressed by MYELOID CELLS and some ENDOTHELIAL CELLS, and were originally characterized based on their ability to bind acetylated LOW-DENSITY LIPOPROTEINS. They can also bind a variety of other polyanionic ligand. Certain scavenger receptors can internalize micro-organisms as well as apoptotic cells.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Macrophages, Peritoneal: Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.Anticholesteremic Agents: Substances used to lower plasma CHOLESTEROL levels.Triolein: (Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Cysteamine: 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.Lipolysis: The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.High-Density Lipoproteins, Pre-beta: A highly dense subclass of the high-density lipoproteins, with particle sizes below 7 nm. They are also known as nascent HDL, composed of a few APOLIPOPROTEIN A-I molecules which are complexed with PHOSPHOLIPIDS. The lipid-poor pre-beta-HDL particles serve as progenitors of HDL3 and then HDL2 after absorption of free cholesterol from cell membranes, cholesterol esterification, and acquisition of apolipoproteins A-II, Cs, and E. Pre-beta-HDL initiate the reverse cholesterol transport process from cells to liver.Heparin Lyase: 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.Aryldialkylphosphatase: An enzyme which catalyzes the hydrolysis of an aryl-dialkyl phosphate to form dialkyl phosphate and an aryl alcohol. It can hydrolyze a broad spectrum of organophosphate substrates and a number of aromatic carboxylic acid esters. It may also mediate an enzymatic protection of LOW DENSITY LIPOPROTEINS against oxidative modification and the consequent series of events leading to ATHEROMA formation. The enzyme was previously regarded to be identical with Arylesterase (EC 3.1.1.2).Electrophoresis, Agar Gel: Electrophoresis in which agar or agarose gel is used as the diffusion medium.Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.Phosphatidylcholines: Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a choline moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and choline and 2 moles of fatty acids.Biological Transport: The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.Hypolipidemic Agents: Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.tau Proteins: 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).Chylomicron Remnants: Metabolic products of chylomicron particles in which TRIGLYCERIDES have been selectively removed by the LIPOPROTEIN LIPASE. These remnants carry dietary lipids in the blood and are cholesterol-rich. Their interactions with MACROPHAGES; ENDOTHELIAL CELLS; and SMOOTH MUSCLE CELLS in the artery wall can lead to ATHEROSCLEROSIS.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Cytidine Deaminase: An enzyme that catalyzes the deamination of cytidine, forming uridine. EC 3.5.4.5.Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Dyslipidemias: Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.Heparin: A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.Coronary Disease: An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.Abetalipoproteinemia: An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.Protein Structure, Secondary: The level of protein structure in which regular hydrogen-bond interactions within contiguous stretches of polypeptide chain give rise to alpha helices, beta strands (which align to form beta sheets) or other types of coils. This is the first folding level of protein conformation.Amyloid: A fibrous protein complex that consists of proteins folded into a specific cross beta-pleated sheet structure. This fibrillar structure has been found as an alternative folding pattern for a variety of functional proteins. Deposits of amyloid in the form of AMYLOID PLAQUES are associated with a variety of degenerative diseases. The amyloid structure has also been found in a number of functional proteins that are unrelated to disease.Antigens, CD36: Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.Circular Dichroism: A change from planar to elliptic polarization when an initially plane-polarized light wave traverses an optically active medium. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Mice, Mutant Strains: Mice bearing mutant genes which are phenotypically expressed in the animals.Emulsions: 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.RNA Editing: A process that changes the nucleotide sequence of mRNA from that of the DNA template encoding it. Some major classes of RNA editing are as follows: 1, the conversion of cytosine to uracil in mRNA; 2, the addition of variable number of guanines at pre-determined sites; and 3, the addition and deletion of uracils, templated by guide-RNAs (RNA, GUIDE).Immunoblotting: Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.Heterozygote Detection: Identification of genetic carriers for a given trait.Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Mild Cognitive Impairment: 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 Factors: 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.Receptors, Immunologic: 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.Binding, Competitive: The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.Carotid Arteries: Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.Vascular Cell Adhesion Molecule-1: Cytokine-induced cell adhesion molecule present on activated endothelial cells, tissue macrophages, dendritic cells, bone marrow fibroblasts, myoblasts, and myotubes. It is important for the recruitment of leukocytes to sites of inflammation. (From Pigott & Power, The Adhesion Molecule FactsBook, 1993, p154)Postprandial Period: The time frame after a meal or FOOD INTAKE.Pedigree: The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.Sterol O-Acyltransferase: An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.Nephelometry and Turbidimetry: Chemical analysis based on the phenomenon whereby light, passing through a medium with dispersed particles of a different refractive index from that of the medium, is attenuated in intensity by scattering. In turbidimetry, the intensity of light transmitted through the medium, the unscattered light, is measured. In nephelometry, the intensity of the scattered light is measured, usually, but not necessarily, at right angles to the incident light beam.Genetic Testing: 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.Cognition: Intellectual or mental process whereby an organism obtains knowledge.Diet: Regular course of eating and drinking adopted by a person or animal.Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Xanthomatosis: 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, Electron: Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.Lecithin Acyltransferase Deficiency: An autosomal recessively inherited disorder caused by mutation of LECITHIN CHOLESTEROL ACYLTRANSFERASE that facilitates the esterification of lipoprotein cholesterol and subsequent removal from peripheral tissues to the liver. This defect results in low HDL-cholesterol level in blood and accumulation of free cholesterol in tissue leading to a triad of CORNEAL OPACITY, hemolytic anemia (ANEMIA, HEMOLYTIC), and PROTEINURIA.Cohort Studies: 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.Sex Factors: 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.Astrocytes: 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.Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.Fasting: Abstaining from all food.Inflammation: 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, Gel: Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.Probucol: A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).Tunica Intima: The innermost layer of an artery or vein, made up of one layer of endothelial cells and supported by an internal elastic lamina.Cell Adhesion Molecules, Neuronal: 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.Aorta, Thoracic: The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.Amyloidosis, Familial: Diseases in which there is a familial pattern of AMYLOIDOSIS.Monocytes: 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.Hepatocytes: The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.DNA Primers: Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.Gene Knock-In 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.Sex Characteristics: 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.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Peptides: Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.Promoter Regions, Genetic: DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.

Competition of Abeta amyloid peptide and apolipoprotein E for receptor-mediated endocytosis. (1/343)

The genetic polymorphism of apolipoprotein E (apoE) is associated with the age of onset and relative risk of Alzheimer's disease (AD). In contrast to apoE3, the wild type allele, apoE4 confers an increased risk of late-onset AD. We demonstrate that the beta-amyloid peptide isoforms Abeta (1-28), Abeta (1-40), and Abeta (1-43) compete for the cellular metabolism of apoE3 and apoE4 containing beta-very low density lipoproteins. An antibody raised against Abeta (1-28) cross-reacted with recombinant apoE. Epitope mapping revealed positive amino acid clusters as common epitopes of Abeta (13 through 17; HHQKL) and apoE (residues 144 through 148; LRKRL), both regions known to be heparin binding domains. Abeta in which amino acids 13 through 17 (HHQKL) were replaced by glycine (GGQGL) failed to compete with the cellular uptake of apoE enriched betaVLDL. These observations indicate that Abeta and apoE are taken up into cells by a common pathway involving heparan sulfate proteoglycans.  (+info)

Apo E phenotype and changes in serum lipids in adult patients during growth hormone replacement. (2/343)

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)

Comparison of the LDL-receptor binding of VLDL and LDL from apoE4 and apoE3 homozygotes. (3/343)

Compared with apolipoprotein E3 (apoE3), apoE2 is less effective in mediating the binding of lipoproteins to the low-density lipoprotein (LDL) receptor. The influence of the E4 isoform, which is associated with adverse effects on plasma lipids and coronary heart disease, is less clear. We compared the ability of very low density lipoprotein (VLDL) and LDL from paired E4/4 and E3/3 subjects to compete against 125I-labeled LDL for binding with the LDL receptor on cultured fibroblasts and Hep G2 cells. The concentrations of VLDL or LDL required to inhibit binding of 125I-LDL by 50% (IC50, microgram apoB/ml) were determined, and results were assessed in terms of an IC50 ratio, E4/4 IC50 relative to E3/3 IC50, to reduce the influence of interassay variability. In Hep G2 cells, E4/4 VLDL was more effective than E3/3 VLDL in competing for the LDL receptor, the IC50 ratio being lower than unity (0.73 +/- 0.31, P < 0.05, two-tailed t-test). IC50 values themselves were marginally lower in E4/4 than E3/3 subjects (3.7 +/- 1.3 vs. 6.1 +/- 3.7, P < 0.08). However, there was no difference between E4/4 and E3/3 VLDL in competing for the LDL receptor on fibroblasts or between E4/4 and E3/3 LDL in competing for the LDL receptor on either cell type. These results suggest that inheritance of apoE4 is associated with an increased affinity of VLDL particles for LDL receptors on hepatocytes and may partly explain the influence of the E4 isoform on lipid metabolism.  (+info)

Binding of beta-VLDL to heparan sulfate proteoglycans requires lipoprotein lipase, whereas ApoE only modulates binding affinity. (4/343)

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. (5/343)

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)

Expression of human apolipoprotein E3 or E4 in the brains of Apoe-/- mice: isoform-specific effects on neurodegeneration. (6/343)

Apolipoprotein (apo) E isoforms are key determinants of susceptibility to Alzheimer's disease. The apoE4 isoform is the major known genetic risk factor for this disease and is also associated with poor outcome after acute head trauma or stroke. To test the hypothesis that apoE3, but not apoE4, protects against age-related and excitotoxin-induced neurodegeneration, we analyzed apoE knockout (Apoe-/-) mice expressing similar levels of human apoE3 or apoE4 in the brain under control of the neuron-specific enolase promoter. Neuronal apoE expression was widespread in the brains of these mice. Kainic acid-challenged wild-type or Apoe-/- mice had a significant loss of synaptophysin-positive presynaptic terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus, and a disruption of neurofilament-positive axons in the hippocampus. Expression of apoE3, but not of apoE4, protected against this excitotoxin-induced neuronal damage. ApoE3, but not apoE4, also protected against the age-dependent neurodegeneration seen in Apoe-/- mice. These differences in the effects of apoE isoforms on neuronal integrity may relate to the increased risk of Alzheimer's disease and to the poor outcome after head trauma and stroke associated with apoE4 in humans.  (+info)

Age-dependent association of apolipoprotein E genotype with coronary and aortic atherosclerosis in middle-aged men: an autopsy study. (7/343)

BACKGROUND: Apolipoprotein E (apoE) polymorphism is one of the genetic determinants of serum cholesterol values. The apoE epsilon4 allele has been associated with advanced coronary heart disease (CHD) diagnosed by angiography, but the role of the apoE genotype in atherosclerosis has not been confirmed at vessel-wall level, nor is any age-dependent effect of the apoE genotype on the development of CHD known. METHODS AND RESULTS: The right and left anterior descending coronary arteries (RCA and LAD) and the aorta from 700 male autopsy cases (Helsinki Sudden Death Study) in 1981-1982 and 1991-1992 (average age 53 years, range 33 to 70 years) were stained for fat, and all areas covered with fatty streaks, fibrotic plaques, and complicated lesions were measured. In the RCA and LAD, the apoE genotype was significantly associated with the area of total atherosclerotic lesions in men <53 years old but not with that in older men (P=0.0085 and P=0.041, respectively, for age-by-genotype interaction). Men <53 years old with the epsilon4/3 genotype showed 61% larger total atherosclerotic lesion area in the RCA (P=0.0027) and 26% larger area in the LAD (P=0.12) than did men with the epsilon3/3. The apoE epsilon4/3 was also associated with atherosclerotic lesions in the abdominal (P=0.014) and thoracic (P=0.12) aorta, but this effect, unlike that of the coronary arteries, was not age-related. CONCLUSIONS: In men, the apoE epsilon4 allele is a significant genetic risk factor for coronary atherosclerosis in early middle age. This suggests that at older age, other known risk factors of CHD play a more important role in the atherosclerotic process than apoE polymorphisms.  (+info)

Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men. (8/343)

BACKGROUND: Alimentary lipemia has been associated with coronary heart disease and common carotid artery intima-media thickness (IMT). This study was designed to investigate the relations of subclasses of postprandial triglyceride-rich lipoproteins (TRLs) with IMT. METHODS AND RESULTS: Ninety-six healthy 50-year-old men with an apolipoprotein (apo) E3/E3 genotype underwent an oral fat tolerance test and B-mode carotid ultrasound examination. The apo B-48 and apo B-100 contents of each fraction of TRLs were determined as a measure of chylomicron remnant and VLDL particle concentrations. In the fasting state, LDL cholesterol (P<0.05) and basal proinsulin (P<0. 05) were significantly related to IMT, whereas HDL cholesterol, plasma triglycerides, and insulin were not. In the postprandial state, plasma triglycerides at 1 to 4 hours (P<0.01 at 2 hours), total triglyceride area under the curve (AUC) (P<0.05), incremental triglyceride AUC (P<0.01), and the large VLDL (Sf 60 to 400 apo B-100) concentration at 3 hours (P<0.05) were significantly related to IMT. Multivariate analyses showed that plasma triglycerides at 2 hours, LDL cholesterol, and basal proinsulin were consistently and independently related to IMT when cumulative tobacco consumption, alcohol intake, waist-to-hip circumference ratio, and systolic blood pressure were included as confounders. CONCLUSIONS: These results provide further evidence for postprandial triglyceridemia as an independent risk factor for early atherosclerosis and also suggest that the postprandial triglyceridemia is a better predictor of IMT than particle concentrations of individual TRLs.  (+info)

*APOA4

... and polymorphisms of the human apolipoprotein A4 gene (APOA4)". Proceedings of the National Academy of Sciences of the United ... Karathanasis SK (1985). "Apolipoprotein multigene family: tandem organization of human apolipoprotein AI, CIII, and AIV genes ... "Genetic polymorphism of human plasma apolipoprotein A-IV is due to nucleotide substitutions in the apolipoprotein A-IV gene". J ... Apolipoprotein A-IV (also known as apoA-IV, apoAIV, or apoA4) is plasma protein that is the product of the human gene APOA4. ...

*APOA5

"Hyperlipidemia in patients with apolipoprotein E 2/2 phenotype: apolipoprotein A5 S19W mutation as a cofactor". Clinical ... Yin YW, Sun QQ, Wang PJ, Qiao L, Hu AM, Liu HL, Wang Q, Hou ZZ (2014-01-01). "Genetic polymorphism of apolipoprotein A5 gene ... Kao JT, Wen HC, Chien KL, Hsu HC, Lin SW (October 2003). "A novel genetic variant in the apolipoprotein A5 gene is associated ... The gene for apolipoprotein A5 (APOA5, gene ID 116519, OMIM accession number - 606368) was originally found by comparative ...

*Apolipoprotein E

Moriyama K, Sasaki J, Matsunaga A, Arakawa F, Takada Y, Araki K, Kaneko S, Arakawa K (September 1992). "Apolipoprotein E1 Lys- ... Apolipoprotein E is a fat-binding protein (apolipoprotein) that is part of the chylomicron and Intermediate-density lipoprotein ... The gene, APOE, is mapped to chromosome 19 in a cluster with apolipoprotein C1 (APOC-I) and the apolipoprotein C2. The APOE ... "Genetic studies of human apolipoproteins. X. The effect of the apolipoprotein E polymorphism on quantitative levels of ...

*Apolipoprotein C3

... and polymorphisms of the human apolipoprotein A4 gene (APOA4)". Proceedings of the National Academy of Sciences of the United ... Karathanasis SK (Oct 1985). "Apolipoprotein multigene family: tandem organization of human apolipoprotein AI, CIII, and AIV ... Apolipoprotein C-III also known as apo-CIII is a protein that in humans is encoded by the APOC3 gene. Apo-CIII is a component ... Apolipoprotein C-III at the US National Library of Medicine Medical Subject Headings (MeSH) Human APOC3 genome location and ...

*Simin Liu

Associations of the apolipoprotein A1/C3/A4/A5 gene cluster with triglyceride and HDL cholesterol levels in women with type 2 ... A prospective study of the APOA1 XmnI and APOC3 SstI polymorphisms in the APOA1/C3/A4 gene cluster and risk of incident ... PMC 1181919 Song Y, Stampfer MJ, Liu S. Meta-analysis: apolipoprotein E genotypes and risk for coronary heart disease. Ann ...

*Apolipoprotein

ApoA1 and ApoA4 are part of the APOA1/C3/A4/A5 gene cluster on chromosome 11. Hundreds of genetic polymorphisms of the ... Apolipoprotein synthesis in the intestine is regulated principally by the fat content of the diet. Apolipoprotein synthesis in ... There are also intermediate-density lipoproteins formed by Apolipoprotein E. There are six classes of apolipoproteins and ... variation in the APOA1/C3/A4/A5 gene cluster". Hum. Genet. 115 (1): 36-56. doi:10.1007/s00439-004-1106-x. PMID 15108119. ...

*Chromosome 19 (human)

Gene map locus 19q13.12 BCKDHA: Branched chain keto acid dehydrogenase E1, alpha polypeptide (maple syrup urine disease). Gene ... map location 19q13.1-q13.2 APOE: Apolipoprotein E, gene associated with Alzheimer's disease. Gene map locus 19q13.2 CIC: ...

*Japanese Americans

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 ...

*Reelin

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 (Aug 2003). "Differential binding of ligands to the apolipoprotein E receptor 2 ... Herz J, Beffert U (Oct 2000). "Apolipoprotein E receptors: linking brain development and Alzheimer's disease". Nature Reviews. ...

*Nutritional genomics

E3) alleles receiving equivalent amounts of dietary fat. One single nucleotide polymorphism (-75 G/A) in the apolipoprotein A1 ... Genetic variations in genes encoding for apolipoproteins, some enzymes and hormones can alter individual sensitivity to ... Individuals with the E4 allele in the apolipoprotein E gene show higher low-density lipoprotein-cholesterol (bad cholesterol) ... levels with increased dietary fat intake compared with those with the other (E1, E2, ...

*APOBEC4

A recent study on APOBEC4 (A4) revealed an interesting finding that A4 enhanced the replication of HIV-1 through boosting ... "Entrez Gene: apolipoprotein B mRNA editing enzyme". Marino D, Perković M, Hain A, Jaguva Vasudevan AA, Hofmann H, Hanschmann KM ... Biochemical analysis of A4 showed the lack of cytidine deaminase activity on single stranded DNA and it binds DNA rather weak. ... C->U-editing enzyme APOBEC-4, also known as Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 4, is a protein ...

*APOBEC3C

"Entrez Gene: APOBEC3C apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3C". Yu Q, Chen D, König R, Mariani R, ... Conversely, A3 proteins enzymatically convert cytidine to uridine present in the single stranded DNA. The crystal structure of ... A3C belong to the A3 family of cytidine deaminases that act as restriction factors against diverse retroviruses. A3C was ...

*Endothelin 2

200 (2): 209.e1-27. doi:10.1016/j.ajog.2008.08.051. PMID 19019335. Grimshaw MJ, Hagemann T, Ayhan A, Gillett CE, Binder C, ... "Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip". American Journal of ...

*X chromosome

APOO: encoding protein Apolipoprotein O ARMCX6: encoding protein Armadillo repeat containing X-linked 6 BEX1: encoding protein ... member A5 CXorf36: encoding protein hypothetical protein LOC79742 CXorf40A: Chromosome X open reading frame 40 CXorf49: ...

*Biochemistry of Alzheimer's disease

By the time Alzheimer's has been diagnosed, DCGM occurs in genotypes APOE3/E4, APOE3/E3, and APOE4/E4. Thus, DCGM is a ... 1997). "No difference in cerebral glucose metabolism in patients with Alzheimer disease and differing apolipoprotein E ... such as patients homozygous for the epsilon 4 variant of the apolipoprotein E gene (APOE4, a genetic risk factor for ...

*CPA3

Carboxypeptidase A3 (mast cell carboxypeptidase A), also known as CPA3, is an enzyme which in humans is encoded by the CPA3 ... Sequential degradation of apolipoprotein B by granule chymase and carboxypeptidase A". The Journal of Biological Chemistry. 261 ... Huang H, Reed CP, Zhang JS, Shridhar V, Wang L, Smith DI (June 1999). "Carboxypeptidase A3 (CPA3): a novel gene highly induced ... including the apolipoprotein B component of LDL particles and angiotensin Ⅰ. Upon mast cell activation and degranulation, CPA3 ...

*APBB1

Amyloid beta A4 precursor protein-binding family B member 1 is a protein that in humans is encoded by the APBB1 gene. The ... Trommsdorff M, Borg JP, Margolis B, Herz J (1999). "Interaction of cytosolic adaptor proteins with neuronal apolipoprotein E ... "Entrez Gene: APBB1 amyloid beta (A4) precursor protein-binding, family B, member 1 (Fe65)". Guénette SY, Chen J, Jondro PD, ... "Interaction of cytosolic adaptor proteins with neuronal apolipoprotein E receptors and the amyloid precursor protein". J. Biol ...

*Amyloid precursor protein

The extracellular region, much larger than the intracellular region, is divided into the E1 and E2 domains, linked by an acidic ... Barger SW, DeWall KM, Liu L, Mrak RE, Griffin WS (Aug 2008). "Relationships between expression of apolipoprotein E and beta- ... A4) precursor protein (peptidase nexin-II, Alzheimer disease) Human APP genome location and APP gene details page in the UCSC ... the complete E1 domain and the E2 domain. APP undergoes extensive post-translational modification including glycosylation, ...

*C4

... the envelope size matching the A4 paper size C-4, the US Army designation of the Ford Trimotor AEG C.IV, a German World War I ... a chess opening Biology Apolipoprotein C4, a human gene ATC code C04 Peripheral vasodilators, a subgroup of the Anatomical ...

*Chromosome 6 (human)

... ubiquitin protein ligase E3 component n-recognin 2 (6p21.2) UNC5CL: encoding protein Unc-5 homolog C (C. elegans)-like VEGF: ... encoding protein Apolipoprotein M (6p21.33) C6orf10: encoding protein Uncharacterized protein C6orf10 (6p21.32) C6orf62: ... E3 ubiquitin protein ligase 1 (6q21) HEBP2: heme binding protein 2 (6q24.1) IFNGR: interferon-γ receptor gene (6q23-q24) IGF2R ... NHL repeat containing E3 ubiquitin protein ligase 1 (6p22.3) NOL7: nucleolar protein 7 (6p23) NQO2: N- ...

*Monoclonal antibody therapy

The A4 study on older individuals who are positive for indicators of AD but are negative for genetic risk factors will test ... However, in patients with increased apolipoprotein (APOE) e4 carriers, Bapineuzumab treatment is also accompanied by vasogenic ... This includes anti-AB treatment in Asymptomatic Alzheimer's Disease (A4), the Alzheimer's Prevention Initiative (API), and DIAN ...

*AMFR

2004). "The gene product of the gp78/AMFR ubiquitin E3 ligase cDNA is selectively recognized by the 3F3A antibody within a ... results in increased ubiquitinylation and decreased secretion of apolipoprotein B100 in HepG2 cells". J. Biol. Chem. 278 (26): ... 2006). "The activity of a human endoplasmic reticulum-associated degradation E3, gp78, requires its Cue domain, RING finger, ...

*Mothers against decapentaplegic homolog 2

Lin X, Liang M, Feng XH (November 2000). "Smurf2 is a ubiquitin E3 ligase mediating proteasome-dependent degradation of Smad2 ... Zannis VI, Kan HY, Kritis A, Zanni E, Kardassis D (March 2001). "Transcriptional regulation of the human apolipoprotein genes ...

*CYP27A1

doi:10.1161/01.ATV.0000022600.61391.A5. PMID 12117727. Meir K, Kitsberg D, Alkalay I, Szafer F, Rosen H, Shpitzen S, Avi LB, ... "Overexpression of steroidogenic acute regulatory protein increases macrophage cholesterol efflux to apolipoprotein AI". ...

*Chromosome 12 (human)

... encoding protein Apolipoprotein F APOLD1: apolipoprotein L domain containing 1 ARL6IP4: encoding protein ADP-ribosylation-like ... encoding enzyme E3 ubiquitin-protein ligase RNF34 SARNP: SAP domain-containing ribonucleoprotein Serpina3f: encoding protein ...

*Dementia with Lewy bodies

As with Alzheimer's disease, the DLB risk is heightened with inheritance of the ε4 allele of the apolipoprotein E (APOE). In ... "Pierre Lalonde est décédé à l'âge de 75 ans". Le Journal de Montréal. Retrieved 2016-06-22. "Pierre Lalonde souffrait aussi de ... la démence à corps de Lewy". Le Journal de Montréal. Retrieved 2016-06-22. "Archived copy". Archived from the original on 2017- ...
In the present study, the expression and causal involvement of MCP-1 in the development of IH in a mouse in vivo or a human ex vivo model of vein graft disease is demonstrated. MCP-1 expression was shown to be present in the murine vein graft and was also detectable in a HSV organ culture. Blocking the CCR2/MCP-1 pathway, using the receptor antagonist 7ND-MCP-1, resulted in a reduced vein graft thickening in both the murine vein graft and in HSV segments. Furthermore, we demonstrate that reduced vein graft thickening, besides the effect on monocyte chemotaxis, is caused by a direct antiproliferative effect of 7ND-MCP-1 on vascular SMCs.. Vein graft thickening attributable to development of IH and accelerated atherosclerosis is the major limitation in the long-term survival of patent vein grafts. The mechanism of vein graft thickening development is largely unknown, but it is assumed that it is caused by an inflammatory response to damage of the graft.9,10. MCP-1 is a well-known proinflammatory ...
Periods of rapid growth seen during the early stages of fetal development, including cell proliferation and differentiation, are greatly influenced by the maternal environment. We demonstrate here that over-nutrition, specifically exposure to a high fat diet in utero, programmed the extent of atherosclerosis in the offspring of ApoE*3 Leiden transgenic mice. Pregnant ApoE*3 Leiden mice were fed either a control chow diet (2.8% fat, n=12) or a high-fat, moderate-cholesterol diet (MHF, 19.4% fat, n=12). Dams were fed the chow diet during the suckling period. At 28d postnatal age wild type and ApoE*3 Leiden offspring from chow or MHF-fed mothers were fed either a control chow diet (n=37) or a diet rich in cocoa butter (15%) and cholesterol (0.25%), for 14 weeks to induce atherosclerosis (n=36). Offspring from MHF-fed mothers had 1.9-fold larger atherosclerotic lesions (p,0.001). There was no direct effect of prenatal diet on plasma triglycerides or cholesterol, however transgenic ApoE*3 Leiden ...
One of the most important steps in atherogenesis is the transition of a fatty streak into an atherosclerotic plaque. In the present study, it was demonstrated that fatty streaks were characterized by DNA synthesis with no detectable apoptosis. These lesions progress toward atherosclerotic plaques, which were characterized by the presence of both DNA synthesis and apoptosis. This finding is comparable to the classic studies of Virchow, who described atherosclerosis as a formative process, starting with "proliferation" and terminating with "fatty degeneration."13 So far, few human data on DNA synthesis during the entire process of atherogenesis are available.14 Orekhov et al14 report peak levels of DNA synthesis in lipid-rich lesions, whereas DNA synthesis in fibrous lesions is much lower. The majority of data on DNA synthesis in human atherosclerosis are confined to advanced lesions only. They show low levels of DNA synthesis (0% to 2%),15 16 17 18 but this level is significantly higher than in ...
Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with vascular amyloid deposition.
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ApoE belongs to a group of proteins that bind reversibly with lipoprotein and play an important role in lipid metabolism.  In addition
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. ...
In this study, we examined Abca1 gene dose effect on the phenotype of APP transgenic mice expressing human ApoE3 or ApoE4 isoforms. Surprisingly, our results demonstrate that the lack of one copy of Abca1 significantly aggravates memory deficits and amyloid pathology in APP/E4 but not in APP/E3 mice. An important finding of the study was that Aβ clearance from the brain was decreased by Abca1 deficiency in APP/E4/Abca1−/+ but not in APP/E3/Abca1−/+ mice. In contrast, Abca1 deficiency did not affect cognition, amyloid phenotype, and Aβ clearance in APP mice expressing ApoE3. Interestingly, the correlation between plasma HDL and brain amyloid load (Fig. 7) suggests that there may be a causative connection between peripheral lipoproteins and Aβ load in the CNS.. Previous studies demonstrated that ABCA1 affects amyloid deposition and memory deficits in experimental animals (Hirsch-Reinshagen et al., 2005; Koldamova et al., 2005b; Wahrle et al., 2005; Lefterov et al., 2009). Furthermore, ...
Cafestol, a diterpene present in unfiltered coffee, potently increases serum cholesterol levels in humans. So far, no suitable animal model has been found to study the biochemical background of this effect. We determined the effect of cafestol on serum cholesterol and triglycerides in different mouse strains and subsequently studied its mechanism of action in apolipoprotein (apo) E*3-Leiden transgenic mice. ApoE*3-Leiden, heterozygous low density lipoprotein-receptor (LDLR+/-) knockout, or wild-type (WT) C57BL/6 mice were fed a high- (0.05% wt/wt) or a low- (0.01% wt/wt) cafestol diet or a placebo diet for 8 weeks. Standardized to energy intake, these amounts are equal to 40, 8, or 0 cups of unfiltered coffee per 10 MJ per day in humans. In apoE*3-Leiden mice, serum cholesterol was statistically significantly increased by 33% on the low- and by 61% on the high-cafestol diet. In LDLR+/- and WT mice, the increases were 20% and 24%, respectively, on the low- cafestol diet and 55% and 46%, ...
TY - JOUR. T1 - Avian and murine lr8b and human apolipoprotein E receptor 2. T2 - Differentially spliced products from corresponding genes. AU - Brandes, Christian. AU - Novak, Sabine. AU - Stockinger, Walter. AU - Herz, Joachim. AU - Schneider, Wolfgang J.. AU - Nimpf, Johannes. PY - 1997/6/1. Y1 - 1997/6/1. N2 - Apolipoprotein E-mediated lipid metabolism in the central nervous system plays an important role in cholesterol and phospholipid homeostasis of this organ, which is separated from the circulation by the blood-brain barrier. Moreover, in late-onset familial Alzheimer disease the frequency of the apolipoprotein E4 allele is significantly increased and the apoprotein is localized to extracellular plaques, one of the histological hallmarks of this disease. Recently, two distinct novel members of the low-density lipoprotein (LDL) receptor family, with the potential to bind apolipoprotein E and preferentially expressed in brain, have been characterized from human (D. Kim et al., 1996, J. ...
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
Compelling and widely accepted genetic evidence shows that the presence of one or more APOE4 genes is associated with more severe disease in Alzheimers, stroke, traumatic brain injury, multiple sclerosis, and many others. The question is, How does APOE4/ApoE4 protein contribute to disease or conversely, how does the absence of APOE3/ApoE3 protein contribute to disease? The likely explanations are quantity and quality of ApoE differs between APOE4 carriers and non-APOE4 carriers (i.e., APOE3 carriers). Riddell and colleagues confirm, as we had previously reported (Vitek et al., 2007), that the amount of ApoE protein in APOE4/4 targeted replacement (TR) mice appears to be significantly less than in their APOE3/3 counterparts. Thus, like many diseases where some critical factor is reduced in the disease, a critical therapeutic path becomes supplementation of that missing critical factor with either the authentic protein or a mimetic of that protein.. But in the case of ApoE, amount is not the ...
Studies using PKC regulatory/catalytic domain chimeras have underscored the complexity of PKC functions in relation to its structural domains. In previous reports, we and others showed that certain features of isozyme-specific PKC functions could be attributed to the catalytic domain only. These include the PKC-δ-mediated PMA-induced macrophage differentiation of 32D cells (14), the tumorigenicity of PKC-ε-overexpressing NIH 3T3 cells (15), the PKC-βII-mediated growth promotion in K-562 cells (26), and the protection of PKC-δ from down-regulation induced by bryostatin 1 in NIH 3T3 cells (17). However, in some cases, both the regulatory and the catalytic domains contribute to the isoform-specific effects (15, 18, 27). Further mapping of the structural domains beyond the catalytic and regulatory regions is essential to clearly determine the function of each structural domain and to understand how individual domains interact with each other to regulate PKC function.. Previous studies on the ...
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Despite apolipoprotein Es important role in cholesterol transport and metabolism in the brain as well as its influence on Alzheimers disease, the impact of the human APOE genotype on cholesterol metabolism in brain has not been fully examined. This study was carried out to investigate APOE genotype effects on oxysterols measured. In this study the measurement of cholesterol and several oxysterols in the brains of human APOE ε2, ε3 and ε4 knock-in mice at 8 weeks and 1 year of age using gas chromatography mass spectrometry (GC-MS) demonstrated no APOE genotype or age effect on total brain cholesterol and the oxysterol 24-hydroxycholesterol. The level of 27-hydroxycholesterol was elevated in 1 year old animals for all APOE genotypes. Interestingly, lathosterol an indicator of cholesterol synthesis was significantly reduced in the 1 year old animals for all APOE genotypes. APOE ε4 expressing mice exhibited statistically lower levels of lathosterol compared to APOE ε2 in both the young and ...
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
The lipid transport protein, apolipoprotein E (apoE), is expressed in many peripheral tissues in vivo including the adrenal gland and testes. To investigate the role of apoE in adrenal cholesterol homeostasis, we have expressed a human apoE genomic clone in the Y1 mouse adrenocortical cell line. Y1 cells do not express endogenous apoE mRNA or protein. Expression of apoE in Y1 cells resulted in a dramatic decrease in basal steroidogenesis; secretion of fluorogenic steroid was reduced 7- to greater than 100-fold relative to Y1 parent cells. Addition of 5-cholesten-3 beta,25-diol failed to overcome the suppression of steroidogenesis in these cells. Cholesterol esterification under basal conditions, as measured by the production of cholesteryl [14C]oleate, was similar in the Y1 parent and the apoE-transfected cell lines. Upon incubation with adrenocorticotropin or dibutyryl cAMP, production of cholesteryl [14C]oleate decreased 5-fold in the Y1 parent cells but was unchanged in the apoE-transfected ...
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 ...
...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
January 15, 2006. In a scientific paper published today a team of scientists from deCODE genetics (Nasdaq:DCGN) and colleagues report the discovery of a variant in a gene on chromosome 10 that represents the most significant genetic risk factor for type 2 diabetes (T2D) found to date. More than one third of individuals in the populations studied carry one copy of the at-risk variant and are at an approximately 45% increased risk of the disease compared to controls; 7% carry two copies and are at a 141% greater risk. The original finding was made in Iceland and was subsequently confirmed in studies in Denmark and the United States. The paper is published today in the online edition of Nature Genetics at www.nature.com/ng, and will appear in the journals February print edition.. "This is a milestone in human genetics. A common gene variant conferring elevated risk of T2D has been earnestly sought by the genetics community for many years. We have found such a variant, which we estimate accounts ...
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。
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.
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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.. ...
APOE (Human) ELISA Kit is an enzyme-linked immunosorbent assay for the quantitative measurement of human APOE2/APOE3/APOE4. (KA4736) - Products - Abnova
Director of the J. David Gladstone Institutes, cardiologist Robert Mahley, a leading expert on apoE, calls the study an important research observation. "It indicates that there may be subgroups of patients who respond differently to statins, and this is especially interesting in relation to the continuing search for the mechanisms of apoE." As yet, F rgeman admits, the researchers "cannot explain our findings in terms of the underlying biology." One initial hypothesis was that there was a connection to patients levels of cholesterol and other lipids in the blood, but data analysis revealed this was not the case. The team now suspects the apoE protein to be involved in some malignant pathogenic processes that lead to coronary death. Results of earlier studies have suggested that e4 carriers are particularly prone to develop disseminated coronary lesions. "We think it most likely that our observations reflect an ability of statin treatment to inhibit the progression of such lesions in e4 ...
Nanoparticles that transport medicines to a specific part of the human body are usually broken down in the liver prematurely. Jeroen Bussmann from Leiden University has discovered a new method to prevent this from happening. Publication in ACS Nano.
APOE formation and its role in redistribution of lipids to the cells of CNS: the neuropathological effects of the neurotoxic APOE fragments.Notes: ① APOE main
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Exposure to radiation can lead to deficits in cognitive function, including impairments in hippocampal-dependent learning and memory. However, not all individuals exposed to irradiation develop cognitive impairments, suggesting the involvement of genetic risk factors. Apolipoprotein E (apoE), a protein important for neuronal repair, might influence susceptibility to developing radiation-induced cognitive impairments. Humans express three major apoE isoforms, apoE2, apoE3 and apoE4. Compared to apoE3, apoE4 increases the risk to develop Alzheimers disease while apoE2 decreases this risk. ApoE4 is also associated with cognitive deficits following neurotrauma. Moreover, deficiency of apolipoprotein E (apoE) in mice worsens cognitive impairments following irradiation. There might also be sex differences in the risk for developing radiation-induced cognitive impairments. In both humans and rodents, females are more susceptible to the effects of irradiation on cognition than males. The neur
Role of apolipoprotein E in neurodegenerative diseases Vo Van Giau,1 Eva Bagyinszky,1 Seong Soo A An,1 SangYun Kim2 1Department of Bionano Technology, Gachon Medical Research Institute, Gachon University, Seongnam, South Korea; 2Department of Neurology, Seoul National University College of Medicine in Seoul National Bundang Hospital, Seoul, South Korea Abstract: Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. APOE-dependent alterations of the endocytic pathway can affect different functions. APOE binds to cell-surface receptors to deliver lipids and to the hydrophobic amyloid-β peptide, regulating amyloid-β aggregations and clearances in the brain. Several APOE isoforms with major structural differences were discovered and shown to influence the brain lipid transport, glucose metabolism, neuronal signaling, neuroinflammation, and mitochondrial function. This review will summarize the updated research progress on APOE functions
Effect of Dietary Fat on LDL Size Influenced by Apolipoprotein E Genotype in Healthy Subjects - posted in Lifestyle: Any thoughts? I read this laymans article here which explains how smaller LDL particle size is a better predictor for increased risk of heart disease, and how high carbohydrate diets decrease the size of LDL particles.The paper below claims the opposite if you are ApoE3/4. Im ApoE3/4, and Ive discussed this topic on longecity before, so I guess Ill contin...
Despite pleiotropic immunomodulatory effects of apolipoprotein E (apoE) in vitro, its effects on the clinical course of experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS) are still controversial. As sex hormones modify immunomodulatory apoE functions, they may explain contentious findings. This study aimed to investigate sex-specific effects of apoE on disease course of EAE and MS. MOG35-55 induced EAE in female and male apoE-deficient mice was assessed clinically and histopathologically. apoE expression was investigated by qPCR. The association of the MS severity score (MSSS) and APOE rs429358 and rs7412 was assessed across 3237 MS patients using linear regression analyses. EAE disease course was slightly attenuated in male apoE-deficient (apoE −/− ) mice compared to wildtype mice (cumulative median score: apoE −/− = 2 [IQR 0.0-4.5];
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
Brain-derived neurotrophic factor (BDNF) is involved in multiple aspects of synaptogenesis, from the formation to the functional maturation of synapses. BDNF influences the morphological complexity of axons and dendrites [15-17], increases synapse number [18-20], modulate synaptic maturation and controls ultrastructural composition of synapses [21, 22]. BDNF is critical for synaptic plasticity and memory processing in adult brain and is also essential to promote short and long term memory [23-26]. BDNF is synthesized as a precursor (pro-BDNF) encompassing two domains, the prodomain and the mature BDNF domain [27]. The pro-BDNF is cleaved by prohormone convertases such as furin and PC1/3 intracellularly or plasminogen/plasmin and MMPs extracellularly [28-30] to release the mature form [31].. Our data show that ApoE2 induces the astrocytes to secrete more m-BDNF than does ApoE3, while ApoE4 produces a negligible amount. We also found that the secreted pro-BDNF level was higher in ApoE3-treated ...
Abstract: This study examined the effects of apolipoprotein E4 (APOE4), the most prevalent genetic risk factor for Alzheimers disease (AD), on proteins involved in mitochondrial dynamics and autophagy, in the hippocampus of targeted replacement mice. Immunohistochemical measurements revealed that the levels of the mitochondrial fusion-mediating protein, MFN1, were higher, whereas those of corresponding fission-regulating protein, DRP-1, were lower in the hippocampus of ApoE4 mice than in the corresponding ApoE3 mice, indicating that APOE4 is associated with increased mitochondrial fusion and decreased fission. A similar ApoE4-driven decrease in DRP-1 was also observed in AD brains. The levels of the mitochondrial proteins COX1 and Tom40, were higher in the ApoE4 mice, which is consistent with the increased fusion. Measurements of the levels of cleaved PINK1 and parkin, which mark and target mitochondria for mitophagic degradation, revealed lower levels of cleaved PINK1, suggesting reduced ...
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Looking for online definition of Leiden in the Medical Dictionary? Leiden explanation free. What is Leiden? Meaning of Leiden medical term. What does Leiden mean?
ARG158CYS; The 3 major isoforms of human apolipoprotein E (apoE2, -E3, and -E4), as identified by isoelectric focusing, are coded for by 3 alleles (epsilon 2, 3, and 4). The E2 (107741.0001), E3 (107741.0015), and E4 (107741.0016) isoforms differ in amino acid sequence at 2 sites, residue 112 (called site A) and residue 158 (called site B). At sites A/B, apoE2, -E3, and -E4 contain cysteine/cysteine, cysteine/arginine, and arginine/arginine, respectively [Weisgraber et al. J. Biol. Chem. 256: 9077-9083 (1981) and Rall et al. Proc. Nat. Acad. Sci. 79: 4696-4700 (1982 ...
Video created by Universiteit Leiden, Leiden University Medical Center for the course Anatomy of the Abdomen and Pelvis; a journey from basis to clinic. . We discussed some microscopy before and the embryonic origin of the initial gut tube and ...
Video created by Universiteit Leiden, Leiden University Medical Center for the course Anatomy of the Abdomen and Pelvis; a journey from basis to clinic. . Welcome to the first week of the course. Have you ever wondered what lies inside your ...
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
Geneticists of Leiden University Medical Center are the first to determine the DNA sequence of a woman. She is also the first European whose DNA sequence has been determined. This has been announced by the researchers this morning, during a special press conference at
Research profile for Eline C. Brombacher (Leids Universitair Medisch Centrum, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.), provided by Rxivist, the site that helps you find the most discussed biology preprints on the internet.
Background: Apolipoprotein E4 (ApoE4) is the major genetic risk factor of Alzheimer’s disease (AD). ApoE4 carriers have cerebral hypometabolism which is thought as a harbinger of AD. Our previous studies indicated ketones improved mitochondria energy metabolism via sirtuin 3 (Sirt3). However, it is unclear whether ketones upregulate Sirt3 and improve ApoE4-related learning and memory deficits.Results: Ketones improved learning and memory abilities of ApoE4 mice but not ApoE3 mice. Sirt3, synaptic proteins, the NAD+/ NADH ratio, and ATP production were significantly increased in the hippocampus and the cortex from ketone treatment.Methods: Human ApoE3 and ApoE4 transgenic mice (9-month-old) were treated with either ketones or normal saline by daily subcutaneous injections for 3 months (ketones, beta-hydroxybutyrate (BHB): 600 mg/kg/day; acetoacetate (ACA): 150 mg/kg/day). Learning and memory ability of these mice were assessed. Sirt3 protein, synaptic proteins (PSD95, Synaptophysin),
TY - JOUR. T1 - Gene-behavior interaction of depressive symptoms and the apolipoprotein e ε4 allele on cognitive decline. AU - Rajan, Kumar. AU - Wilson, Robert S.. AU - Skarupski, Kimberly A.. AU - Mendes De Leon, Carlos F.. AU - Evans, Denis A.. PY - 2014/1/1. Y1 - 2014/1/1. N2 - Objective: Depressive symptoms and the apolipoprotein E (APOE) [Latin Small Letter Open ε4 allele are independent risk factors for cognitive decline. However, it is not clear whether the presence of both depressive symptoms and the APOE [Latin Small Letter Open ε4 allele increases cognitive decline. METHODS: A prospective study of a population-based sample of 4150 (70% African American and 63% women) participants 65 years and older who were interviewed at 3-year intervals was conducted. Depressive symptoms were measured using the 10-item version of the Center for Epidemiologic Studies Depression scale, with each item coded as presence or absence of a symptom. The APOE genotype was ascertained by DNA samples ...
Authors: Blautzik, Janusch , Kotz, Sebastian , Brendel, Matthias , Sauerbeck, Julia , Vettermann, Franziska , Winter, Yaroslav , Bartenstein, Peter , Ishii, Kazunari , Rominger, Axel Article Type: Research Article Abstract: Body weight loss in late-life is known to occur at a very early stage of Alzheimers disease (AD). Apolipoprotein E4 (ApoE4) represents a major genetic risk factor for AD and is linked to an increased cortical amyloid-β (Aβ) accumulation. Since the relationship between body weight, ApoE4, and AD pathology is poorly investigated, we aimed to evaluate whether ApoE4 allelic status modifies the association of body mass index (BMI) with markers of AD pathology. A total of 368 Aβ-positive cognitively healthy or mild cognitive impaired subjects had undergone [18 F]-AV45-PET, [18 F]-FDG-PET, and T1w-MRI examinations. Composite cortical [18 F]-AV45 uptake and …[18 F]-FDG uptake in posterior cingulate cortex were calculated as surrogates of cortical Aβ load and glucose ...
Sporadic, late-onset Alzheimers disease has no known cause and shows no obvious inheritance pattern. However, in some families, clusters of cases are seen. Although a specific gene has not been identified as the cause of late-onset Alzheimers, genetic factors do appear to play a role in the development of this form.. Two risk factor genes have been linked to Alzheimers diseases so far. Researchers have identified an increased risk of developing late-onset Alzheimers related to the apolipoprotein E (APOE) gene found on chromosome 19. The APOE gene comes in several different forms, but three occur most frequently: APOE e2, APOE e3, and APOE e4. People inherit one APOE from each parent. Having the e4 form is a risk factor for Alzheimers disease, but it does not mean that Alzheimers disease will necessarily develop. The e3 form is the most common form found in the general population and may play a neutral role in AD. The rarer e2 form appears to be associated with a lower risk of AD.. The ...
Lipnicki DM; Crawford JD; Dutta R; Thalamuthu A; Kochan NA; Andrews G; Fernanda Lima-Costa M; Castro-Costa E; Brayne C; Matthews FE, 2017, Age-related cognitive decline and associations with sex, education and apolipoprotein E genotype across ethnocultural groups and geographic regions: a collaborative cohort study, PLOS ONE, vol. 12, http://dx.doi.org/10.1371/journal.pmed.1002261. Opel N; Redlich R; Kaehler C; Grotegerd D; Dohm K; Heindel W; Kugel H; Thalamuthu A; Koutsouleris N; Arolt V, 2017, Prefrontal gray matter volume mediates genetic risks for obesity, Molecular Psychiatry, vol. 22, pp. 703 - 710, http://dx.doi.org/10.1038/mp.2017.51. Lipnicki DM; Crawford JD; Dutta R; Thalamuthu A; Kochan NA; Andrews G; Lima-Costa MF; Castro-Costa E; Brayne C; Matthews FE, 2017, Age-related cognitive decline and associations with sex, education and apolipoprotein E genotype across ethnocultural groups and geographic regions: a collaborative cohort study, PLoS Medicine, vol. 14, ...
Martel CL, Mackic JB, Matsubara E, Governale S, Miguel C, Miao W, McComb JG, Frangione B, Ghiso J, Zlokovic BV. Isoform-specific effects of apolipoproteins E2, E3, and E4 on cerebral capillary sequestration and blood-brain barrier transport of circulating Alzheimers amyloid beta ...
A recent article in this month s Archives of General Psychiatry underscores all this hoopla about the Apo E4 alleles. Apolipoprotein E Genotype and Age-Related Mylein Breakdown in Healthy Individuals by George Bartzokis M.D. et al. These authors discuss that In addition to genotype-phenotype associations with vascular disease, the alleles and isoforms of Apo E4 have been related to dementias, most commonly Alzheimer s disease. Apolipoprotein E (APOE) genotype is the most influential Alzheimer disease (AD) risk factor after advanced age. The APOE4 alleles decrease and the APOE2 alleles increase age at onset of AD. Human and nonhuman primate data suggest that in midlife, the structural integrity of myelin sheaths begins breaking down, with an accelerating age-related trajectory most evident in the brains later-myelinating association regions. This may result in a progressive "disconnection" of widely distributed neural networks that may underlie the age risk factor for AD. The authors of this ...
Apolipoprotein (apolipoprotein) je bílkovinná složka lipoproteinů. Apolipoproteinů existuje více druhů a jednotlivé typy se vyskytují v konkrétních lipoproteinech. Apolipoproteiny mají více funkcí, jsou strukturálně důležité, pomáhají transportu lipoproteinových částic, a dokonce mohou fungovat jako koenzymy některých enzymů ...
Interferon-beta (IFN-beta) therapy for multiple sclerosis (MS) is associated with a potential for induction of neutralizing antibodies (NAbs). Because immune reactivity depends on changes in lipoprote
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 Alzheimers disease, res
Molendijk M.L. (3 juni 2014), The role of BDNF in depression. Will the neurothrophin hypothesis sparkle on, long after the glitter of the firework is gone? (Dissertatie. Psychology, Faculty of Social and Behavioural Sciences, Leiden). Promotor(en) en Copromotor(en):Elzinga B.M., Penninx B.W.J.H., Spinhoven P.dissertatie ...
Video created by Universiteit Leiden for the course The Changing Global Order. The topic addressed this week is NATO in a Changing World. There are two lectures by Prof. dr. Rob de Wijk. The first examines coercion and the second elucidates ...
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Leiden Indo-European Etymological Dictionary Series; 10), volume II, with the assistance of Lucien van Beek, Leiden, Boston: Brill, pages 945-946 ...
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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?
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 ...
TY - JOUR. T1 - Binding of apolipoprotein E inhibits the oligomer growth of amyloid-β peptide in solution as determined by fluorescence cross-correlation spectroscopy. AU - Ly, Sonny. AU - Altman, Robin. AU - Petrlova, Jitka. AU - Lin, Yu. AU - Hilt, Silvia. AU - Huser, Thomas R. AU - Laurence, Ted A.. AU - Voss, John C. PY - 2013/4/26. Y1 - 2013/4/26. N2 - One of the primary neuropathological hallmarks of Alzheimer disease is the presence of extracellular amyloid plaques resulting from the aggregation of amyloid-β (Aβ) peptides. The intrinsic disorder of the Aβ peptide drives self-association and progressive reordering of the conformation in solution, and this dynamic distribution of Aβ complicates biophysical studies. This property poses a challenge for understanding the interaction of Aβ with apolipoprotein E (apoE). ApoE plays a pivotal role in the aggregation and clearance of Aβ peptides in the brain, and the ε4 allele of APOE is the most significant known genetic modulator of ...
Apolipoprotein E (apoE) is critical in the modulation of cholesterol and phospholipid transport between cells of different types. Human apoE is a polymorphic protein with three common alleles, APO epsilon 2, APO epsilon 3, and APO epsilon 4. ApoE4 is associated with sporadic and late-onset familial Alzheimer disease (AD). Gene dose was shown to have an effect on risk of developing AD, age of onset, accumulation of senile plaques in the brain, and reduction of choline acetyltransferase (ChAT) activity in the hippocampus of AD subjects. To characterize the possible impact of the apoE4 allele on cholinergic markers in AD, we examined the effect of apoE4 allele copy number on pre- and postsynaptic markers of cholinergic activity. ApoE4 allele copy number showed an inverse relationship with residual brain ChAT activity and nicotinic receptor binding sites in both the hippocampal formation and the temporal cortex of AD subjects. AD cases lacking the apoE4 allele showed ChAT activities close or within ...
The brain has high energy demands, which are met by the complete oxidation of glucose, the obligatory energy substrate for the brain under physiological conditions. Glucose oxidative metabolism consists of cytosolic processes that generate pyruvate, TCA cycle that provides reducing equivalents, and mitochondrial oxidative phosphorylation that converts energy to ATP. Consistent with the crucial role of energy metabolism in the maintenance of brain function, impaired glucose metabolism, and mitochondrial dysfunction have been implicated in the pathobiology of many brain disorders, including Alzheimers disease (AD) and diabetes. In this dissertation, the molecular mechanisms underlying altered glucose metabolism in the brains at genetic risk for AD and perturbed mitochondrial function in diabetes-associated brain dysfunction are studied. In the first study, the impact of human ApoE isoforms, which confer differential risk for AD, on brain glucose metabolism were investigated in human ApoE ...
Reduced testosterone levels have been implicated as a potential causative factor in cognitive decline with older age. Men who possess the apolipoprotein E (APOE) 4 allele have an increased risk of developing Alzheimers disease; however, no studies have examined whether the influence of testosterone on cognition in healthy older men may be modulated by this geneticpredisposition. The objective of the study was to investigate the association between serum testosterone concentrations and cognitive performance in healthy older men, taking into account APOE 4 status. This was a cross-sectional study conducted from 2003 to 2004. The study population consisted of community-dwelling males residing in Perth, Western Australia. Healthy men over 55 yr, free of cognitive impairment and dementia (n = 45), were included in the study. Participants had fasting early morning blood samples for testosterone and SHBG and were assessed for mood as well as indices of general cognition, verbal and visual memory, ...
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 ...
Alleles of the apolipoprotein E (ApoE) gene are known to modulate the genetic risk for developing late-onset Alzheimers disease (AD) and have been associated with hippocampal volume differences in AD. However, the effect of these alleles on hippocam
1OR3: Conformational flexibility in the apolipoprotein E amino-terminal domain structure determined from three new crystal forms: implications for lipid binding.
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References for Abcams Human Apolipoprotein A I peptide (ab66674). Please let us know if you have used this product in your publication
Published on 10/1/2017. Neu SC, Pa J, Kukull W, Beekly D, Kuzma A, Gangadharan P, Wang LS, Romero K, Arneric SP, Redolfi A, Orlandi D, Frisoni GB, Au R, Devine S, Auerbach S, Espinosa A, Boada M, Ruiz A, Johnson SC, Koscik R, Wang JJ, Hsu WC, Chen YL, Toga AW. Apolipoprotein E Genotype and Sex Risk Factors for Alzheimer Disease: A Meta-analysis. JAMA Neurol. 2017 Oct 01; 74(10):1178-1189. PMID: 28846757.. Read at: PubMed ...
Video created by Universiteit Leiden, Leiden University Medical Center for the course Anatomy of the Abdomen and Pelvis; a journey from basis to clinic. . The abdominal body wall and the pelvis are the topics of this week. What happens if you ...
Epsilon polymorphism of apolipoprotein E gene and insertion-deletion polymorphism of ACE gene and brain ischemic stroke in children: association pilot-study ...
Common variants of the ApoE gene are strongly associated with the risk of developing late-onset Alzheimers disease, but the genes role in the disease has been unclear. Now, researchers funded by the National Institutes ...
The ApoE gene may have a more influential role than first thought; it may amplify the damage done by the tau protein, causing neurodegeneration.
Gupta, V., Wilson, A., Burnham, S., Hone, E., Pedrini, S., Laws, S., Lim, F., Rembach, A., Rainey-Smith, S., Ames, D., Cobiac, L., Macaulay, SL., Masters, C., Rowe, C., Bush, A., Martins, R., (2015), Follow-up plasma apolipoprotein E levels in the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing (AIBL) cohort. Alzheimers Research and Therapy, 7(1), Article no.16, United Kingdom, BioMed Central Ltd., DOI: 10.1186/s13195-015-0105-6 ...
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Blood donors of the Madrid area show a 6% frequency of apolipoprotein E genotype carrying allele epsilon 4. This frequency is smaller than other populations of Caucasian origin. This proportion decreases to 4% in a selected sample of healthy individuals of ages | 60 years. The frequency (34%) of the allele epsilon 4 was significantly increased in patients of late onset Alzheimers disease, similarly to other populations. An earlier age of onset of the dementia is observed in the patients of late-onset Alzheimers disease carrying the allele epsilon 4. No increased frequency in allele epsilon 4 frequency was found in patients of early-onset Alzheimers disease. Patients of Parkinsons disease do not show any differences in the frequency of the alleles of apolipoprotein E when compared with healthy individuals.
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
TY - JOUR. T1 - Influence of apolipoprotein e ε4 on rates of cognitive and functional decline in mild cognitive impairment. AU - Whitehair, Danielle C.. AU - Sherzai, Abdullah. AU - Emond, Jennifer. AU - Raman, Rema. AU - Aisen, Paul S.. AU - Petersen, Ronald Carl. AU - Fleisher, Adam S.. PY - 2010/9. Y1 - 2010/9. N2 - Background: Apolipoprotein E ε4 (APOE ε4) allele carrier status has been well established as a risk factor for developing Alzheimers disease. However, the specific influence of APOE ε4 allele status on cognitive and functional rates of decline in mild cognitive impairment (MCI) is poorly understood. We examine the prospective association of APOE ε4 allele status on measures of cognitive and functional decline in subjects with amnestic MCI (aMCI). Methods: A total of 516 aMCI participants aged 55-90 years who received placebo or vitamin E from the Alzheimers Disease Cooperative Studys MCI treatment trial were evaluated. During the 36-month study period, neurocognitive and ...
Alzheimers disease (AD) is characterized by progressive cognitive decline and memory loss. It has been hypothesized that environmental factors and gene-environment interactions (GXE) may increase AD risk and accelerate cognitive decline. However, there is currently little direct evidence supporting this hypothesis. Interestingly, the E4 allele of the Apolipoprotein E gene (ApoE4) is the strongest known genetic risk factor for late-onset, sporadic AD, and it is also associated with accelerated cognitive decline compared to ApoE4 non-carriers. Furthermore, the heavy metal lead is a neurotoxicant of major public health importance and is associated with persistent cognitive and behavior deficits in humans. Using transgenic knock-in (KI) mice that express the human ApoE4 allele (ApoE4-KI), I found that adult-only lead exposure is sufficient to impair cognitive behavior and that lead-exposed ApoE4-KI mice develop more severe or exhibit earlier deficits in learning and memory compared to ApoE3-KI ...
The APOE gene has other symbols as "AD2", "LPG", "APO-E", and "LDLCQ5". It is located at 19q13.2. The APOE gene has important roles in cardiovascular diseases including myocardial infarction, ischemic stroke, and coronary heart disease (Kathiresan et al. 2008).. The APOE gene is involved in immune responses to lipid antigens (Van den Elzen et al. 2005). It has also been connected with Alzheimers disease (Lambert et al. 2002), cognitive impairment (Caselli et al. 2009), multiple sclerosis (MS) (Enzinger et al. 2003).. In addition, it is associated with neurologic disorders such as epilepsy (Busch et al. 2007) and age-related macular degeneration (ARMD) (Anderson et al. 2001).. References:. Anderson, D. H., Ozaki, S., Nealon, M., Neitz, J., Mullins, R. F., Hageman, G. S., Johnson, L. V. Local cellular sources of apolipoprotein E in the human retina and retinal pigmented epithelium: implications for the process of drusen formation. Am. J. Ophthal. 131: 767-781, 2001.. Busch, R. M., Lineweaver, T. ...
There is a well-established association between APOE genotype and the risk of developing Alzheimers disease (AD). Relative to individuals with the common ε3/ε3 genotype, carriers of the ε4 allele are at increased risk of developing AD, while carriers of the ε2 allele appear to be protected against the disease. However, we recently reported that in a sample of cognitively healthy adults, both ε4 and ε2 carriers showed nearly identical changes in the pattern of fMRI activity during memory and non-memory tasks, relative to ε3 homozygotes. These findings suggest that the effects of APOE on brain function are not tightly linked to the effects of this gene on AD risk. Here we test the hypothesis that APOE has an intrinsic effect on the brains functional networks. Resting-state fMRI was used to compare the pattern of functional connectivity of a variety of resting-state networks between 77 cognitively healthy participants aged 32 to 55 with different APOE genotypes (23 ε2/ε3, 20 ε3/ε3, 26 ε3/ε4,
According to a recent study reported in the Neural Regeneration Research, APOE ε4 plays an important role in augmenting cognitive decline, and APOC1 H2 may act synergistically with APOE ε4 in increasing the risk of cognitive decline in Chinese patients with late-onset Alzheimers disease.
Methods and Results-Atherosclerosis development was quantified in 2 lines of transgenic mice expressing human AR (hAR) crossed on the apolipoprotein E knockout background. The transgenes were used to increase the normally low levels of this enzyme in wild-type mice. Both generalized hAR overexpression and hAR expression via the Tie 2 promoter increased lesion size in streptozotocin diabetic mice. In addition, pharmacological inhibition of AR reduced lesion size.. ...
The human apolipoprotein E (APOE) gene is polymorphic, with three primary alleles (E2, E3, E4) that differ at two key non-synonymous sites. These alleles are functionally different in how they bind to lipoproteins, and this genetic variation is associated with phenotypic variation for several medical traits, including cholesterol levels, cardiovascular health, Alzheimers disease risk, and longevity. The relative frequencies of these alleles vary across human populations, and the evolution and maintenance of this diversity is much debated. Previous studies comparing human and chimpanzee APOE sequences found that the chimpanzee sequence is most similar to the human E4 allele, although the resulting chimpanzee protein might function like the protein coded for by the human E3 allele. However, these studies have used sequence data from a single chimpanzee and do not consider whether chimpanzees, like humans, show intra-specific and subspecific variation at this locus. ...
In an animal model, a novel approach toward correct structural problems in apolipoprotein E 4 protein aims to prevent the misfolding, which triggers proteolysis, and the cascade leading to Alzheimers disease.. A new treatment for Alzheimers disease that focuses on correcting the structure of the apolipoprotein E4 (APOE4) protein has been shown to work in mice and could be ready for testing in humans within two years.. The treatment, tentatively named PY-101, would dissolve the bond that causes two domains of the APOE4 protein to fuse within neurons and cause misfolding, which triggers proteolysis. The breakdown of the protein then produces toxic fragments that disrupt mitochondrial function and promote cell death.. This process, rather than the accumulation of amyloid-beta (Abeta) accounts for the strong correlation between the APOE4 allele and numerous neurological disorders, including Alzheimers disease, according to Robert W. Mahley, MD, PhD, president emeritus of the J. David Gladstone ...
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Video created by Universiteit Leiden, Leiden University Medical Center for the course Anatomy of the Abdomen and Pelvis; a journey from basis to clinic. . 2000+ courses from schools like Stanford and Yale - no application required. Build ...
Webster University offers a semester study program in Leiden that is comprised of two sessions lasting 8 weeks each. Students usually take 2-3...
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Ben je 16 jaar of ouder, ben je 1 avond of meerdere avonden in de week beschikbaar (ook op feestdagen) en lijkt het je leuk om in een grote keuken te helpen met ...
We have demonstrated that there is a strong association between polymorphic poly-T variant of TOMM40 and the age of onset of late-onset Alzheimers disease (AD)...
Several studies in mice indicate a role for apolipoprotein E (APOE) in lipid accumulation and adipogenic differentiation in adipose tissue. However, little is yet known if APOE functions in a similar manner in human adipocytes. This prompted us to compare lipid loading and expression of adipocyte differentiation markers in APOE-deficient and control adipocytes using the differentiated human mesenchymal stem cell line hMSC-Tert as well as primary human and mouse adipocytes as model systems. Differentiated hMSC-Tert were stably transduced with or without siRNA targeting APOE while murine adipocytes were isolated from wild type and Apoe knockout mice. Human APOE knockdown hMSC-Tert adipocytes accumulated markedly less triglycerides compared to control cells. This correlated with strongly decreased gene expression levels of adipocyte markers such as adiponectin (ADIPOQ) and fatty acid binding protein 4 (FABP4) as well as the key transcription factor driving adipocyte differentiation, peroxisome ...

Apolipoprotein E3/ApoE3 Antibodies: Novus BiologicalsApolipoprotein E3/ApoE3 Antibodies: Novus Biologicals

Browse our Apolipoprotein E3/ApoE3 Antibody catalog backed by our Guarantee+. ... Apolipoprotein E3/ApoE3 Antibodies available through Novus Biologicals. ... Apolipoprotein E3/ApoE3 Antibodies. We offer Apolipoprotein E3/ApoE3 Antibodies for use in common research applications: ... Choose from our Apolipoprotein E3/ApoE3 polyclonal antibodies and browse our Apolipoprotein E3/ApoE3 monoclonal antibody ...
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Apolipoprotein A5 - Semantic ScholarApolipoprotein A5 - Semantic Scholar

It regulates levels of plasma TRIGLYCERIDES by activating APOLIPOPROTEIN C-II LIPOPROTEIN LIPASE and inhibiting hepatic VLDL ... A minor apolipoprotein that associates with HIGH-DENSITY LIPOPROTEINS (HDL), VERY-LOW-DENSITY LIPOPROTEINS (VLDL), and ... Apolipoprotein A5. Known as: Apo A-V Protein, ApoA-V Protein, Apolipoprotein A-V (More). ... The novel apolipoprotein A5 is present in human serum, is associated with VLDL, HDL, and chylomicrons, and circulates at very ...
more infohttps://www.semanticscholar.org/topic/Apolipoprotein-A5/1041726

RCSB PDB 









- 1OR3: APOLIPOPROTEIN E3 (APOE3), TRIGONAL TRUNCATION MUTANT 165 Structure Summary PageRCSB PDB - 1OR3: APOLIPOPROTEIN E3 (APOE3), TRIGONAL TRUNCATION MUTANT 165 Structure Summary Page

Conformational flexibility in the apolipoprotein E amino-terminal domain structure determined from three new crystal forms: ... PROTEIN (APOLIPOPROTEIN E) A 165 Homo sapiens Fragment: RECEPTOR BINDING DOMAIN Details: SELENOMETHIONINE MUTANT USED IN MAD ...
more infohttp://www.rcsb.org/pdb/explore/explore.do?structureId=1OR3

Biophysical analysis of apolipoprotein E3 variants linked with development of type III hyperlipoproteinemia.  - PubMed - NCBIBiophysical analysis of apolipoprotein E3 variants linked with development of type III hyperlipoproteinemia. - PubMed - NCBI

Biophysical analysis of apolipoprotein E3 variants linked with development of type III hyperlipoproteinemia.. Georgiadou D1, ... Biophysical Analysis of Apolipoprotein E3 Variants Linked with Development of Type III Hyperlipoproteinemia ... Biophysical Analysis of Apolipoprotein E3 Variants Linked with Development of Type III Hyperlipoproteinemia ... Biophysical Analysis of Apolipoprotein E3 Variants Linked with Development of Type III Hyperlipoproteinemia ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/22069485?dopt=Abstract

Apolipoprotein E3- and Nitric Oxide-Dependent Modulation of Endothelial Cell Inflammatory Responses | Arteriosclerosis,...Apolipoprotein E3- and Nitric Oxide-Dependent Modulation of Endothelial Cell Inflammatory Responses | Arteriosclerosis,...

Apolipoprotein E3- and Nitric Oxide-Dependent Modulation of Endothelial Cell Inflammatory Responses. Adam E. Mullick, Andrew F ... Apolipoprotein E3- and Nitric Oxide-Dependent Modulation of Endothelial Cell Inflammatory Responses ... Apolipoprotein E3- and Nitric Oxide-Dependent Modulation of Endothelial Cell Inflammatory Responses ... Apolipoprotein E3- and Nitric Oxide-Dependent Modulation of Endothelial Cell Inflammatory Responses ...
more infohttp://atvb.ahajournals.org/content/early/2006/11/30/01.ATV.0000253947.70438.99

Expression of Human Apolipoprotein E3 or E4 in the Brains ofApoe−/− Mice: Isoform-Specific Effects on Neurodegeneration |...Expression of Human Apolipoprotein E3 or E4 in the Brains ofApoe−/− Mice: Isoform-Specific Effects on Neurodegeneration |...

Expression of Human Apolipoprotein E3 or E4 in the Brains ofApoe−/− Mice: Isoform-Specific Effects on Neurodegeneration. Manuel ... Expression of Human Apolipoprotein E3 or E4 in the Brains ofApoe−/− Mice: Isoform-Specific Effects on Neurodegeneration ... Expression of Human Apolipoprotein E3 or E4 in the Brains ofApoe−/− Mice: Isoform-Specific Effects on Neurodegeneration ... 1996) Human apolipoprotein E2, E3, and E4 isoform-specific transgenic mice: human-like pattern of glial and neuronal ...
more infohttp://www.jneurosci.org/content/19/12/4867?ijkey=b5941efb8950a529a966f846402ba0cfc52f80e0&keytype2=tf_ipsecsha

Identification and Characterization of Cyclic AMP Response Element-Binding Protein H Response Element in the Human...Identification and Characterization of Cyclic AMP Response Element-Binding Protein H Response Element in the Human...

... apolipoprotein A5 (APOA5), was identified by the comparative sequencing of the APOA1/C3/A4 gene cluster region [3]. APOA5, ... N. Vu-Dac, P. Gervois, H. Jakel et al., "Apolipoprotein A5, a crucial determinant of plasma triglyceride levels, is highly ... K.-H. Song, "Orphan nuclear receptor Nur77 participates in human apolipoprotein A5 gene expression," Biochemical and ... M. Nowak, A. Helleboid-Chapman, H. Jakel et al., "Insulin-mediated down-regulation of apolipoprotein A5 gene expression through ...
more infohttps://www.hindawi.com/journals/bmri/2013/892491/

Identification and Characterization of Cyclic AMP Response Element-Binding Protein H Response Element in the Human...Identification and Characterization of Cyclic AMP Response Element-Binding Protein H Response Element in the Human...

N. Vu-Dac, P. Gervois, H. Jakel et al., "Apolipoprotein A5, a crucial determinant of plasma triglyceride levels, is highly ... K.-H. Song, "Orphan nuclear receptor Nur77 participates in human apolipoprotein A5 gene expression," Biochemical and ... M. Nowak, A. Helleboid-Chapman, H. Jakel et al., "Insulin-mediated down-regulation of apolipoprotein A5 gene expression through ... A. Genoux, H. Dehondt, A. Helleboid-Chapman et al., "Transcriptional regulation of apolipoprotein A5 gene expression by the ...
more infohttps://www.hindawi.com/journals/bmri/2013/892491/ref/

A genetic variant c.553G | T (rs2075291) in the apolipoprotein A5 gene is associated with altered triglycerides levels in...A genetic variant c.553G | T (rs2075291) in the apolipoprotein A5 gene is associated with altered triglycerides levels in...

Associations of the apolipoprotein A1/C3/A4/A5 gene cluster with triglyceride and HDL cholesterol levels in women with type 2 ... Several epidemiological studies have shown that apolipoprotein A1/C3/A4/A5 gene cluster is found to be one of the factors that ... Apolipoprotein A1/C3/A5 haplotypes and serum lipid levels. Lipids Health Dis. 2011;10:140.CrossRefGoogle Scholar ... Apolipoprotein A5 and hypertriglyceridemia. Clin Chem. 2005;51(2):295-7.CrossRefGoogle Scholar ...
more infohttps://rd.springer.com/article/10.1186%2Fs12872-018-0965-3

Apolipoprotein A5, a newly identified gene that affects plasma triglyceride levels in humans and mice - DOE Joint Genome...Apolipoprotein A5, a newly identified gene that affects plasma triglyceride levels in humans and mice - DOE Joint Genome...

Apolipoprotein A5 (APOA5) is a newly described member of the apolipoprotein gene family whose initial discovery arose from ... Apolipoprotein A5, a newly identified gene that affects plasma triglyceride levels in humans and mice. Published in:. ... Apolipoprotein A5, a newly identified gene that affects plasma triglyceride levels in humans and mice ... comparative sequence analysis of the mammalian APOA1/C3/A4 gene cluster. Functional studies in mice indicated that alteration ...
more infohttps://jgi.doe.gov/publication/apolipoprotein-a5-a-newly-identified-gene-that-affects-plasma-triglyceride-levels-in-humans-and-mice/

Gestational hyperlipidemia and acute pancreatitis with underlying partial lipoprotein lipase deficiency and apolipoprotein E3...Gestational hyperlipidemia and acute pancreatitis with underlying partial lipoprotein lipase deficiency and apolipoprotein E3...

Gestational hyperlipidemia and acute pancreatitis with underlying partial lipoprotein lipase deficiency and apolipoprotein E3/ ... deficiency but without an associated LPL gene mutation in the presence of the apolipoprotein E3/2 genotype. This is the first ... 3), and her apoE genotype was E3/2. We evaluated the LPL gene on chromosome 8q22, and detected no gene mutation. This test ... She was diagnosed with a partial LPL deficiency without the LPL gene mutation in the presence of the apo E3/2 genotype. Several ...
more infohttp://www.kjim.org/journal/view.php?number=169159

Hepatitis B virus inhibits apolipoprotein A5 expression through its core gene | Lipids in Health and Disease | Full TextHepatitis B virus inhibits apolipoprotein A5 expression through its core gene | Lipids in Health and Disease | Full Text

Apolipoprotein A5 (ApoA5) is a new apolipoprotein family member that plays an important role in the regulation of lipid ... Apolipoprotein A5 (ApoA5) is a new apolipoprotein family member that plays an important role in the regulation of lipid ... Apolipoprotein A5 (ApoA5) is a new member of the apolipoprotein family and is specifically synthesized and secreted by the ... The novel apolipoprotein A5 is present in human serum, is associated with VLDL, HDL, and chylomicrons, and circulates at very ...
more infohttps://lipidworld.biomedcentral.com/articles/10.1186/s12944-016-0340-2

Polymorphism in the promoter region of the apolipoprotein A5 gene is associated with an increased susceptibility for coronary...Polymorphism in the promoter region of the apolipoprotein A5 gene is associated with an increased susceptibility for coronary...

Polymorphism in the promoter region of the apolipoprotein A5 gene is associated with an increased susceptibility for coronary ... Polymorphism in the promoter region of the apolipoprotein A5 gene is associated with an increased susceptibility for coronary ... Polymorphism in the promoter region of the apolipoprotein A5 gene is associated with an increased susceptibility for coronary ... Polymorphism in the promoter region of the apolipoprotein A5 gene is associated with an increased susceptibility for coronary ...
more infohttps://hungary.pure.elsevier.com/en/publications/polymorphism-in-the-promoter-region-of-the-apolipoprotein-a5-gene

Apolipoprotein E3/E3 genotype decreases the risk of pituitary dysfunction after traumatic brain injury due to various causes:...Apolipoprotein E3/E3 genotype decreases the risk of pituitary dysfunction after traumatic brain injury due to various causes:...

Pituitary functions were evaluated, and APO E genotypes (E2/E2; E3/E3; E4/E4; E2/E3; E2/E4; E3/E4) were screened. Twenty-four ... Apolipoprotein E3/E3 genotype decreases the risk of pituitary dysfunction after traumatic brain injury due to various causes: ... The ratio of pituitary dysfunction was significantly lower in subjects with APO E3/E3 (17.7%) than the subjects without APO E3/ ... Present data demonstrated that APO E3/E3 genotype decreases the risk of hypopituitarism after TBI. The demonstration of the ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=38099

Haplotype analysis of the Apolipoprotein A5 gene in Moroccan patients with the metabolic syndrome | Journal of Diabetes &...Haplotype analysis of the Apolipoprotein A5 gene in Moroccan patients with the metabolic syndrome | Journal of Diabetes &...

Associations of the apolipoprotein A1/C3/A4/A5 gene cluster with triglyceride and HDL cholesterol levels in women with type 2 ... Apolipoprotein A5 gene (APOA5) was identified 30 kb upstream of the well-characterized APOA1/C3/A4 gene cluster on chromosome ... Apolipoprotein A5 T-1131C variant confers risk for metabolic syndrome. Pathol Oncol Res POR. 2007;13(3):243-7.View Article ... Kao J-T, Wen H-C, Chien K-L, Hsu H-C, Lin S-W. A novel genetic variant in the apolipoprotein A5 gene is associated with ...
more infohttps://jdmdonline.biomedcentral.com/articles/10.1186/s40200-015-0160-3

The interaction of Apolipoprotein A5 gene promoter region T-1131C polymorphism (rs12286037) and lifestyle modification on...The interaction of Apolipoprotein A5 gene promoter region T-1131C polymorphism (rs12286037) and lifestyle modification on...

BACKGROUND/OBJECTIVE: Apolipoprotein A5 gene promoter region T-1131C polymorphism (APOA5 T-1131C) is known to be associated ... The interaction of Apolipoprotein A5 gene promoter region T-1131C polymorphism (rs12286037) and lifestyle modification on ... The interaction of Apolipoprotein A5 gene promoter region T-1131C polymorphism (rs12286037) and lifestyle modification on ...
more infohttps://ir.lib.shimane-u.ac.jp/ja/list/shimane_creators/N/83d7c5ff8016f1cfaf052a10d48d0702/item/40059

A genetic variant c.553G | T (rs2075291) in the apolipoprotein A5 gene is associated with altered triglycerides levels in...A genetic variant c.553G | T (rs2075291) in the apolipoprotein A5 gene is associated with altered triglycerides levels in...

A genetic variant c.553G , T (rs2075291) in the apolipoprotein A5 gene is associated with altered triglycerides levels in ... A genetic variant c.553G , T (rs2075291) in the apolipoprotein A5 gene is associated with altered triglycerides levels in ... A genetic variant c.553G , T (rs2075291) in the apolipoprotein A5 gene is associated with altered triglycerides levels in ... A genetic variant c.553G , T (rs2075291) in the apolipoprotein A5 gene is associated with altered triglycerides levels in ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=171922

Dietary Intake of n-6 Fatty Acids Modulates Effect of Apolipoprotein A5 Gene on Plasma Fasting Triglycerides, Remnant...Dietary Intake of n-6 Fatty Acids Modulates Effect of Apolipoprotein A5 Gene on Plasma Fasting Triglycerides, Remnant...

Background- Apolipoprotein A5 gene (APOA5) variation is associated with plasma triglycerides (TGs). However, little is known ... Background- Apolipoprotein A5 gene (APOA5) variation is associated with plasma triglycerides (TGs). However, little is known ... Dietary Intake of n-6 Fatty Acids Modulates Effect of Apolipoprotein A5 Gene on Plasma Fasting Triglycerides, Remnant ... Dietary Intake of n-6 Fatty Acids Modulates Effect of Apolipoprotein A5 Gene on Plasma Fasting Triglycerides, Remnant ...
more infohttp://roderic.uv.es/handle/10550/18832

内蒙古快3今天的预测:Sheep Apolipoprotein E(APOE) ELISA kit,AD2, LDLCQ5, LPG, MGC1571, apolipoprotein E3 - ▶内蒙古快3基本走势计内蒙古快3今天的预测:Sheep Apolipoprotein E(APOE) ELISA kit,AD2, LDLCQ5, LPG, MGC1571, apolipoprotein E3 - ▶内蒙古快3基本走势计

Sheep Apolipoprotein E(APOE) ELISA kit,AD2, LDLCQ5, LPG, MGC1571, apolipoprotein E3 ???? ?? ... Apolipoprotein E, a main apoprotein of the chylomicron, binds to a specific receptor on liver cells and peripheral cells. ApoE ... Sheep Apolipoprotein E(APOE) ELISA kit. *. Chylomicron remnants and very low density lipoprotein (VLDL) remnants are rapidly ... Defects in apolipoprotein E result in familial dysbetalipoproteinemia, or type III hyperlipoproteinemia (HLP III), in which ...
more infohttps://www.5qvlr.cn/product/ELISA_Kit/Sheep_Apolipoprotein_E

Product - Page 2 of 90, Research Innate immune response | Genetex Inc.Product - Page 2 of 90, Research 'Innate immune response' | Genetex Inc.

Apolipoprotein A4 antibody Rabbit Polyclonal Hu ELISA, WB (1). GTX17117 Apolipoprotein A4 antibody Rabbit Polyclonal Chk ELISA ...
more infohttp://www.genetex.com/Web/search/Catalog/2?Research=0607

BioLegend - Explore new productsBioLegend - Explore new products

Apolipoproteins (1) APP/β-Amyloid (1) APP/Aβ Degradation (2) Autophagosome Markers (8) Blood Group Markers (4) CD Molecules ( ... Recombinant Human Apolipoprotein E3/APOE3 (carrier-free) BA RUO 786802 10 µg ...
more infohttps://biolegend.com/fr-ch/explore-new-products?GroupID=&PageNum=1&DateReleasedMin=2019-08-27&DateReleasedMax=2020-02-27

Primary antibodies - Page 40 of 867 on g | Genetex Inc.Primary antibodies - Page 40 of 867 on 'g' | Genetex Inc.

Apolipoprotein A5 antibody pair [2G1H11 and 1F1E8] Mouse Monoclonal Hu ELISA, WB ... Apolipoprotein B antibody [6G6] Mouse Monoclonal Hu ELISA, FACS, ICC/IF, WB ... Apolipoprotein M antibody [10C3G5] Mouse Monoclonal Hu, Mk ELISA, ICC/IF, WB ...
more infohttp://www.genetex.com/Web/Search/Catalog/40?Category=494&Keyword=g

Current Drug Targets, Volume 16 - Number 12Current Drug Targets, Volume 16 - Number 12

Apolipoprotein A5: Extracellular and Intracellular Roles in Triglyceride Metabolism. , 16(12): 1274 - 1280. Trudy M. Forte and ...
more infohttps://benthamscience.com/journals/current-drug-targets/volume/16/issue/12/

Recombinant Human Apolipoprotein E (ab50244) | AbcamRecombinant Human Apolipoprotein E (ab50244) | Abcam

Buy our Recombinant Human Apolipoprotein E. Ab50244 is a full length protein produced in Escherichia coli and has been ... Belongs to the apolipoprotein A1/A4/E family.. * Post-translational. modifications. Synthesized with the sialic acid attached ... A fast and cost-effective method for apolipoprotein E isotyping as an alternative to APOE genotyping for patient screening and ...
more infohttps://www.abcam.com/recombinant-human-apolipoprotein-e-ab50244.html

Cancers  | Free Full-Text | Signal-Targeted Therapies and Resistance Mechanisms in Pancreatic Cancer: Future Developments...Cancers | Free Full-Text | Signal-Targeted Therapies and Resistance Mechanisms in Pancreatic Cancer: Future Developments...

established recently, from a large-cohort study of 500 patient sera, a panel of two proteins, apolipoprotein A4 (APOA4) and ... Lin, C.; Wu, W.C.; Zhao, G.C.; Wang, D.S.; Lou, W.H.; Jin, D.Y. ITRAQ-based quantitative proteomics reveals apolipoprotein A-I ... Honda et al., recently developed an antibody-based assay (ELISA) to measure circulating apolipoprotein A2 (APOA2) isoforms ... for detection of early stage pancreatic cancer and risk factors for pancreatic malignancy using antibodies for apolipoprotein- ...
more infohttps://www.mdpi.com/2072-6694/10/6/174/htm
  • We offer Apolipoprotein E3/ApoE3 Antibodies for use in common research applications: Immunocytochemistry, Immunohistochemistry, Simple Western, Western Blot. (novusbio.com)
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