Apolipoprotein C-I: A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.Apolipoproteins C: A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.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).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.TriglyceridesApolipoprotein A-I: The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.Apolipoproteins E: A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.Apolipoprotein B-100: A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.Apolipoproteins B: Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.Apolipoprotein E4: A major and the second most common isoform of apolipoprotein E. In humans, Apo E4 differs from APOLIPOPROTEIN E3 at only one residue 112 (cysteine is replaced by arginine), and exhibits a lower resistance to denaturation and greater propensity to form folded intermediates. Apo E4 is a risk factor for ALZHEIMER DISEASE and CARDIOVASCULAR DISEASES.Apolipoprotein E3: A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.Apolipoprotein A-II: The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.Apolipoproteins: Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.Apolipoprotein C-II: A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.Apolipoproteins A: Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.Apolipoprotein B-48: A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.Apolipoprotein E2: One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.Lipoproteins, HDL: A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.Apoprotein(a): A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Lipoproteins: Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.Lipoprotein(a): A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.Apolipoproteins D: A glycoprotein component of HIGH-DENSITY LIPOPROTEINS that transports small hydrophobic ligands including CHOLESTEROL and STEROLS. It occurs in the macromolecular complex with LECITHIN CHOLESTEROL ACYLTRANSFERASE. Apo D is expressed in and secreted from a variety of tissues such as liver, placenta, brain tissue and others.Lipoproteins, LDL: A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.Lipids: A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)Receptors, LDL: Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Cholesterol, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.Arteriosclerosis: Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Phosphatidylcholine-Sterol O-Acyltransferase: An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).Influenzavirus A: A genus in the family ORTHOMYXOVIRIDAE causing influenza and other diseases in humans and animals. It contains many strains as well as antigenic subtypes of the integral membrane proteins hemagglutinin (HEMAGGLUTININS) and NEURAMINIDASE. The type species is INFLUENZA A VIRUS.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Antibody Specificity: The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.Goats: Any of numerous agile, hollow-horned RUMINANTS of the genus Capra, in the family Bovidae, closely related to the SHEEP.Antibodies, Bacterial: Immunoglobulins produced in a response to BACTERIAL ANTIGENS.Antibodies, Viral: Immunoglobulins produced in response to VIRAL ANTIGENS.Isoantibodies: Antibodies from an individual that react with ISOANTIGENS of another individual of the same species.Fluorescein-5-isothiocyanate: Fluorescent probe capable of being conjugated to tissue and proteins. It is used as a label in fluorescent antibody staining procedures as well as protein- and amino acid-binding techniques.Denervation: The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)Visible Human Projects: Digital image data sets, consisting of complete, anatomically detailed, three-dimensional representations of the normal male and female human bodies.Sympathectomy: The removal or interruption of some part of the sympathetic nervous system for therapeutic or research purposes.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.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.Olfactory Bulb: Ovoid body resting on the CRIBRIFORM PLATE of the ethmoid bone where the OLFACTORY NERVE terminates. The olfactory bulb contains several types of nerve cells including the mitral cells, on whose DENDRITES the olfactory nerve synapses, forming the olfactory glomeruli. The accessory olfactory bulb, which receives the projection from the VOMERONASAL ORGAN via the vomeronasal nerve, is also included here.Cerebellum: The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.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.Immunoassay: A technique using antibodies for identifying or quantifying a substance. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance.Spectrometry, Mass, Electrospray Ionization: A mass spectrometry technique used for analysis of nonvolatile compounds such as proteins and macromolecules. The technique involves preparing electrically charged droplets from analyte molecules dissolved in solvent. The electrically charged droplets enter a vacuum chamber where the solvent is evaporated. Evaporation of solvent reduces the droplet size, thereby increasing the coulombic repulsion within the droplet. As the charged droplets get smaller, the excess charge within them causes them to disintegrate and release analyte molecules. The volatilized analyte molecules are then analyzed by mass spectrometry.Mass Spectrometry: An analytical method used in determining the identity of a chemical based on its mass using mass analyzers/mass spectrometers.

Mass spectral study of polymorphism of the apolipoproteins of very low density lipoprotein. (1/189)

New isoforms of apolipoprotein (apo)C-I and apoC-III have been detected in delipidated fractions from very low density lipoprotein (VLDL) using matrix-assisted laser desorption (MALDI) and electrospray ionization (ESI) mass spectrometry (MS). The cleavage sites of truncated apoC-III isoforms have also been identified. The VLDL fractions were isolated by fixed-angle single-spin ultracentrifugation using a self-generating sucrose density gradient and delipidated using a newly developed C18 solid phase extraction protocol. Fifteen apoC isoforms and apoE were identified in the MALDI spectra and the existence of the more abundant species was verified by ESI-MS. The relative intensities of the apoCs are closely correlated in three normolipidemic subjects. A fourth subject with type V hyperlipidemia exhibited an elevated apoC-III level and a suppressed level of the newly discovered truncated apoC-I isoform. ApoC-II was found to be particularly sensitive to in vitro oxidation. The dynamic range and specificity of the MALDI assay shows that the complete apoC isoform profile and apoE phenotype can be obtained in a single measurement from the delipidated VLDL fraction.  (+info)

A thymidine to cytosine substitution for codon 26 of exon 3 of apolipoprotein C-II gene in a patient with apolipoprotein C-II deficiency. (2/189)

A 52-year-old Japanese woman was evaluated for severe hypertriglyceridemia and recurrent acute pancreatitis. This hypertriglyceridemia was found to be due to the absence of serum apolipoprotein C-II (apo C-II) which was identified by Western blotting using polyclonal anti-apo C-II antiserum. DNA sequence analysis of the apo C-II gene from the patient revealed a homozygous nucleotide change: a thymidine (T) to cytosine (C) substitution in codon 26 (TGG->CGG) at the third exon of the apo C-II gene, that resulted in a Trp26 to Arg substitution. The mutation was also confirmed by restriction fragment length polymorphism (RFLP) analysis with the restriction enzyme Hpa II. The same mutation has been found in a case previously reported in Japan, and was named apo C-II Wakayama. However, the case in Wakayama prefecture showed two concomitant point mutations at the 5'-flanking region upstream from the first exon, which were not identified in our case by RFLP analysis with the restriction enzyme BstXI. Considering that the prefectures of these two cases, Nara and Wakayama, are next to each other, the mutation in our case may be a genetic forebear of apo C-II Wakayama. However, no familial relationship between the two cases has been documented.  (+info)

Protective effect of apolipoprotein A I, A II, C I and C II on endothelial cells injury induced by low density lipoprotein. (3/189)

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

Fibrinolytic factors, serum lipid and C-reactive protein predicting cardiac events in Japanese patients with coronary atherosclerotic lesions. (4/189)

Although disturbances of the fibrinolytic system and serum lipid, and the presence of inflammation, may be risk factors for coronary artery disease (CAD), few reports have investigated these relationships in Japanese patients. Data on 106 patients (79 men and 27 women, mean age 62.3 years) with atherosclerotic lesions on the coronary angiogram were evaluated prospectively to identify whether the factors were useful in predicting the risk of coronary events during a follow-up of 50+/-4 months. Of the 106 patients who were followed, 11 patients had coronary events (4 acute myocardial infarction and 7 unstable angina pectoris). In univariate Cox analyses, a high level of tissue-plasminogen activator (t-PA), apolipoprotein CII, C-reactive protein (CRP), and a low level of high-density lipoprotein-cholesterol (HDL-C) was each associated with a significant increase in the risk of future cardiac events. The stepwise model of Cox proportional hazards analysis selected only a high level of t-PA and CRP as predictors of cardiac events. Controlling for any risk factor did not lower the relation between t-PA and the risk of cardiac events, whereas the relative risk of cardiac events in CRP was not significant when controlled for HDL-C. Thus, in prospective data obtained from a cohort of Japanese patients with coronary atherosclerotic lesions, the elevation of t-PA was an independent predictor of subsequent cardiac events. The prognostic role of CRP in cardiac events was related to a low level of HDL-C.  (+info)

Structure of a biologically active fragment of human serum apolipoprotein C-II in the presence of sodium dodecyl sulfate and dodecylphosphocholine. (5/189)

We have studied the three-dimensional structure of a biologically active peptide of apolipoprotein C-II (apoC-II) in the presence of lipid mimetics by CD and NMR spectroscopy. This peptide, corresponding to residues 44-79 of apoC-II, has been shown to reverse the symptoms of genetic apoC-II deficiency in a human subject. A comparison of alpha-proton secondary shifts and CD spectroscopic data indicates that the structure of apoC-II(44-79) is similar in the presence of dodecylphosphocholine and sodium dodecyl sulfate. The three-dimensional structure of apoC-II(44-79) in the presence of sodium dodecyl sulfate, determined by relaxation matrix calculations, contains two amphipathic helical domains formed by residues 50-58 and 67-75, separated by a non-helical linker centered at Tyr63. The C-terminal helix is terminated by a loop formed by residues 76-79. The C-terminal helix is better defined and has a larger hydrophobic face than the N-terminal helix, which leads us to propose that the C-terminal helix together with the non-helical Ile66 constitute the primary lipid binding domain of apoC-II(44-79). Based on our structure we suggest a new mechanism of lipoprotein lipase activation in which both helices of apoC-II(44-79) remain lipid bound, while the seven-residue interhelical linker extends away from the lipid surface in order to project Tyr63 into the apoC-II binding site of lipoprotein lipase.  (+info)

In addition to the high-density lipoprotein fraction, apolipoprotein C-III is detected in chylomicrons and the very low-density lipoprotein fraction from serum of normolipidemic cows. (6/189)

Apolipoprotein (apo) C-III is a low-molecular-mass protein that is involved in the regulation of the triglyceride metabolism. Except for the hyperlipidemic calf, cattle apoC-III is mainly detected in the high-density lipoprotein (HDL) fraction, and the distribution in chylomicrons (CM) and the very low-density lipoprotein (VLDL) fraction has not yet been clarified. The purpose of the present study was to detect apoC-III in concentrated CM and VLDL fractions to examine whether apoC-III is distributed in the two fractions even in normolipidemic cattle. ApoC-III could be detected by immunoblot analysis in both concentrated cow CM and VLDL fractions, but not in the corresponding calf fractions. These results suggest that apoC-III is distributed in the CM and VLDL fractions, at least in cows, although the concentrations in these fractions are considerably lower than in the HDL fraction.  (+info)

Expression of the apolipoprotein C-II gene during myelomonocytic differentiation of human leukemic cells. (7/189)

Apolipoprotein C-II (apoC-II), which is known to activate lipoprotein lipase (LPL), was identified by ordered differential display (ODD)-polymerase chain reaction (PCR) as a cDNA fragment exhibiting a distinct increase in expression during 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced differentiation of promonocytic U937 cells into monocytes and macrophages. The amount of apoC-II mRNA expression detectable in U937 cells significantly increased and reached a maximum 24-48 h after treatment with 32 nM TPA. apoC-II mRNA was also detected in monocytic THP-1 cells but was not detected in promyelocytic HL-60 cells. In healthy human tissues, the most significant expression of apoC-II mRNA was in the liver. Although apoC-II mRNA expression was markedly up-regulated during the induced differentiation of HL-60 cells into monocytes and macrophages with 32 nM TPA, such expression was not induced during the differentiation of HL-60 cells into granulocytes with 1.25% dimethyl sulfoxide. These results suggest that human apoC-II expression is induced at the transcription level during myelomonocytic differentiation and may confer an important role to macrophages involved in normal lipid metabolism and atherosclerosis.  (+info)

Sub-micellar phospholipid accelerates amyloid formation by apolipoprotein C-II. (8/189)

Lipid-free human apolipoprotein C-II (apoC-II) forms amyloid fibrils with characteristic beta-structure. This conformation is distinct from the alpha-helical fold of lipid-bound apoC-II. We have investigated the effect of the short-chain phospholipid, dihexanoylphosphatidylcholine (DHPC) on amyloid formation by apoC-II. The alpha-helical content of apoC-II increases in the presence of micellar DHPC (16 mM) and amyloid formation is inhibited. However, at sub-micellar DHPC concentrations (below 8 mM) amyloid formation is accelerated 6 fold. These results suggest that individual phospholipid molecules in vivo may exert significant effects on amyloid folding pathways.  (+info)

The self-assembly of specific proteins to form insoluble amyloid fibrils is a characteristic feature of a number of age-related and debilitating diseases. Lipid-free human apolipoprotein C-II (apoC-II) forms characteristic amyloid fibrils and is one of several apolipoproteins that accumulate in amyloid deposits located within atherosclerotic plaques. X-ray diffraction analysis of aligned apoC-II fibrils indicated a simple cross-beta-structure composed of two parallel beta-sheets. Examination of apoC-II fibrils using transmission electron microscopy, scanning transmission electron microscopy, and atomic force microscopy indicated that the fibrils are flat ribbons composed of one apoC-II molecule per 4.7-A rise of the cross-beta-structure. Cross-linking results using single-cysteine substitution mutants are consistent with a parallel in-register structural model for apoC-II fibrils. Fluorescence resonance energy transfer analysis of apoC-II fibrils labeled with specific fluorophores provided ...
Amyloid fibrils have historically been characterized by diagnostic dye-binding assays, their fibrillar morphology, and a cross-beta x-ray diffraction pattern. Whereas the latter demonstrates that amyloid fibrils have a common beta-sheet core structure, they display a substantial degree of morphological variation. One striking example is the remarkable ability of human apolipoprotein C-II amyloid fibrils to circularize and form closed rings. Here we explore in detail the structure of apoC-II amyloid fibrils using electron microscopy, atomic force microscopy, and x-ray diffraction studies. Our results suggest a model for apoC-II fibrils as ribbons approximately 2.1-nm thick and 13-nm wide with a helical repeat distance of 53 nm +/- 12 nm. We propose that the ribbons are highly flexible with a persistence length of 36 nm. We use these observed biophysical properties to model the apoC-II amyloid fibrils either as wormlike chains or using a random-walk approach, and confirm that the probability of ring
Apolipoprotein C-II deficiency (APOC2) Test Cost INR 30000.00 Surat Pune Jaipur Lucknow Kanpur Nagpur Visakhapatnam Indore Thane Bhopal Patna Vadodara Ghaziabad Ludhiana Coimbatore Madurai Meerut Ranchi Allahabad Trivandrum Pondicherry Mysore Aligarh best offer discount price
Distribution of apolipoprotein C-II mRNA and protein in the perinatal mouse lung. Mouse tissue sections are from saccular stage (A, B, H, GD 19.5; C, G, PN 0; I
Order monoclonal and polyclonal Apolipoprotein C-II antibodies for many applications. Selected quality suppliers for anti-Apolipoprotein C-II antibodies.
Cholesterol and triglyceride test - Animation Maybe youve been eating fast food more often than you should, or youre not getting your recommended two-and-a-half hours of exercise each week. Or, it could be that you smoke, or your blood pressure is too high. Well, for whatever reason, you may be concerned about your risk of getting heart disease. Well, a few tests can help you learn that risk, so you can start making healthy lifestyle changes to reduce it. A coronary risk profile is a group of blood tests that measure your cholesterol and triglyceride levels. Why is it important to know these levels? Because if you have too much of these substances in your blood from eating foods like burgers and French fries, they can clog your arteries. Eventually your arteries can become so clogged that youll have a heart attack or stroke. Men should have their cholesterol tested by the time theyre 35. Women should have it checked by age 45. If you have a condition like diabetes, heart disease, stroke, or ...
Rabbit polyclonal Apolipoprotein CII antibody validated for WB, IHC, ICC/IF and tested in Human. Referenced in 1 publication and 2 independent reviews…
Creative Biolabs provides Lenti-C2 CAR (scFv-CD28, CIIC1; M2139) Viral Particle product for Biopharmaceutical research,preclinical and clinical trials.
Collagen II antibody [CIIC1] (collagen, type II, alpha 1) for IA, IHC-Fr, IHC-P, Functional Assay. Anti-Collagen II mAb (GTX54398) is tested in Mouse, Chicken, Rat, Baboon, Horse samples. 100% Ab-Assurance.
UCL Discovery is UCLs open access repository, showcasing and providing access to UCL research outputs from all UCL disciplines.
Apolipoprotein C2 or apolipoprotein C-II is a protein that in humans is encoded by the APOC2 gene. secreted in plasma where it is a component of very low density lipoproteins and chylomicrons. This protein activates the enzyme lipoprotein lipase in capillaries,[5] which hydrolyzes triglycerides and thus provides free fatty acids for cells. Mutations in this gene cause hyperlipoproteinemia type IB, characterized by xanthomas, pancreatitis, and hepatosplenomegaly, but no increased risk for atherosclerosis. Lab tests will show elevated blood levels of triglycerides, cholesterol, and chylomicrons[6] ...
Looking for online definition of ApoC-II in the Medical Dictionary? ApoC-II explanation free. What is ApoC-II? Meaning of ApoC-II medical term. What does ApoC-II mean?
Get an answer for For how long can a C-II drug prescription be filled after it is prescribed?I want to know the time period controlled drugs can filled in the pharmacy after it has been prescribed. and find homework help for other Health questions at eNotes
Good morning! CIIC is pleased to announce the publication of its latest inspection report, on the re-inspection of Toledo Correctional Institution (TOCI). The TOCI inspection and subsequent report was one of the most concerning of the biennium, but I am very pleased to say that TOCI has made an extraordinary transformation in the past year. In the 2013 inspection, a number of concerns were raised regarding a high number of inmate deaths, healthcare services, security, management of the maximum security inmate population, and others. Following the CIIC inspection report (and the DRCs internal concerns), the DRC made large changes in the institution, including shifts in administrative personnel, decreasing the inmate population, increasing staff, consulting outside experts, and essentially conducting a top-to-bottom review. The positive results were immediately apparent. TOCI has improved in almost every area.. The institution is overall safer, with a perceptibly more secure environment. ...
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details ...
Both active and passive connectivity associated with significant improvement in patient-reported perceptions of overall health, disease outlook and emotional well-being
and the therapeutic and commercial potential of WAYLIVRA and other products in development. Any statement describing Ionis or Akceas goals, expectations, financial or other projections, intentions or beliefs, including the commercial potential of TEGSEDI, WAYLIVRA or other of Ionis or Akceas drugs in development is a forward-looking statement and should be considered an at-risk statement. Such statements are subject to certain risks and uncertainties, particularly those inherent in the process of discovering, developing and commercializing drugs that are safe and effective for use as human therapeutics, and in the endeavor of building a business around such drugs. Ionis and Akceas forward-looking statements also involve assumptions that, if they never materialize or prove correct, could cause its results to differ materially from those expressed or implied by such forward-looking statements. Although Ionis and Akceas forward-looking statements reflect the good faith judgment of its ...
RAPOSO, HELENA F.... Apolipoprotein CIII overexpression exacerbates diet-induced obesity due to adipose tissue higher exogenous lipid uptake and retention and lower lipolysis rates. NUTRITION & METABOLISM 12 n. p. DEC 23 2015. Journal article.
C H Bolton, A P Corfield, L G Downs; Sialidase Activity Acting on Apolipoprotein CIII 1 and 2 in Human Leukocytes and Platelets. Clin Sci (Lond) 1 January 1984; 67 (s9): 15P. doi: https://doi.org/10.1042/cs067015P. Download citation file:. ...
TY - JOUR. T1 - Implication of substrate-assisted catalysis on improving lipase activity or enantioselectivity in organic solvents. AU - Tsai, Shau Wei. AU - Chen, Chun Chi. AU - Yang, Hung Shien. AU - Ng, I. Son. AU - Chen, Teh Liang. PY - 2006/8/1. Y1 - 2006/8/1. N2 - In comparison with the biocatalyst engineering and medium engineering approaches, very few examples have been reported on using the substrate engineering approach such as substrate-assisted catalysis (SAC) for naturally occurring or engineered lipases and serine proteases to improve the enzyme activity and enantioselectivity. By employing lipase-catalyzed hydrolysis of (R,S)-naproxen esters in water-saturated isooctane as the model system, we demonstrate the proton shuttle device to the leaving alcohol of the substrate as a new means of SAC to effectively improve the lipase activity or enantioselectivity. The result cannot only provide a strong evidence for the rate-limiting proton transfer for the bond-breaking of tetrahedron ...
Rabbit polyclonal Apolipoprotein CIII antibody validated for WB, ELISA, ICC/IF, sELISA and tested in Human. Referenced in 3 publications. Immunogen…
Familial chylomicronemia syndrome (FCS) is a serious disease that prevents the body from breaking down fats.. Eating even a little fat can make someone with FCS ill, and the condition causes chronic symptoms and can lead to potentially fatal pancreatitis. FCS is a genetic disorder passed down from parents. Because it is rare, many healthcare providers have never heard of FCS or may not know how to diagnose it.. Lipoprotein lipase is a digestive enzyme that helps the body break down structures called chylomicrons. People who have FCS have a problem with lipoprotein lipase: it is either missing or broken. Chylomicrons carry triglycerides (a type of fat) to where they are needed in the body for energy. A buildup of these particles causes an increase in triglycerides levels.. Patients with FCS have extremely high levels of triglycerides. Normal triglyceride levels fall below 150 mg/dL. For people with FCS, triglyceride levels can exceed 1,000 mg/dL, even after medication and/or a low-fat diet are ...
Apolipoproteins have important structural and functional roles in several lipoprotein particles. Apolipoproteins regulate lipid metabolism, adipose tissue, and energy production and serve major...
Gentaur molecular products has all kinds of products like :search , Alpha Dia \ Anti_Human Plasma Apolipoprotein A_I protein antiserum \ APOA11-S for more molecular products just contact us
... from Kaseey Industry co.,ltd on Manufacturer.com. This supplier is located in Shijiazhuang, China in the province of Hebei.
Discover the latest in beauty at Sephora. Explore our unrivaled selection of makeup, skin care, fragrance and more from classic and emerging brands
Discover the latest in beauty at Sephora. Explore our unrivaled selection of makeup, skin care, fragrance and more from classic and emerging brands
25I-NBOH (NBOH-2CI, Cimbi-27) je fenetilaminski halucinogen. On deluje kao potentan agonist 5HT2A receptora,[1][2] sa Ki od 0,061 nM na ljudskom 5HT2A receptoru, te je dvanaest puta potentniji od liganda 2C-I. In vitro testovi su pokazali da ovo jedinjenje deluje kao agonist, ali rezultati životinjskih studija nisu objavljeni. Dok su N-benzilni derivati 2C-I liganda znatno povećavali potentnost, N-benzil derivati 2,5-dimetoksi-4-jodoamfetamina su neaktivni.[3] ...
WELCOME to the 103rd Season of the TOK-cok, SING-song, FOOD-Loving, BBB-spreading & Cat-Loving thread! Earlier threads - EXPOSE yourself - I EXPOSE yourself - II EXPOSE yourself - III EXPOSE yourself - IV EXPOSE yourself - V EXPOSE yourself - VI
WELCOME to the 103rd Season of the TOK-cok, SING-song, FOOD-Loving, BBB-spreading & Cat-Loving thread! Earlier threads - EXPOSE yourself - I EXPOSE yourself - II EXPOSE yourself - III EXPOSE yourself - IV EXPOSE yourself - V EXPOSE yourself - VI
PERFECT TIMING - CAR WASH - WHEN IS THE MOST PERFECT TIME TO WASH YOUR CAR? UNDER THE RAIN? HAHAHA. WHY USE A HOSE TO CLEAN IF YOU CAN CLEAN WITH RAINWATER? THIS GUY IS FUNNY. MORE FU... ...
TY - JOUR. T1 - Purification of biologically active apolipoproteins by chromatofocussing. AU - McLeod, Roger. AU - Lacko, Andras G.. AU - Pritchard, P. Haydn. AU - Frohlich, Jiri. PY - 1986/1/1. Y1 - 1986/1/1. N2 - Chromatofocussing has been used to isolate homogeneous apolipoproteins (apo) from human very-low-density lipoproteins and high-density lipoproteins with protein recovery of 70%. The inclusion of sulfhydryl-reducing agent (dithiothreitol) was required during solubilization of the lipoproteins (following delipidation) to achieve reproducible elution profiles. Removal of polyvalent buffers from apoproteins was rapidly accomplished on small columns of hydroxylapatite. The biological activity of purified apo AI and apo CII was confirmed by assessment of their ability to activate lecithin:cholesterol acyltransferase or lipoprotein lipase, respectively. Functional properties of isolated apo E were assessed by in vitro interaction with the low-density lipoprotein receptor expressed by ...
no scale, but i want to dose between 20-25mg. i used to eyeball 2c-t-7 doses by dividing the 100mg of powder into ~equal piles...suggestions? (feel free to suggest anything regarding 2c-i...doesnt
Going green isnt possible without integrated systems and efficient design, and it has just gotten easier. Under a program recently developed by the U.S ...
The objective of the present study was to determine whether information about a biometrically inferred single gene with large effects on erythrocyte sodium-lithium countertransport is useful in predicting the probability of having hypertension. We used multivariate logistic regression to model the relationship between the probability of having hypertension and predictor traits in a sample of 382 unrelated adult women and 347 unrelated adult men from Rochester, Minn. First, we identified a set of demographic, biochemical, and physiological predictors. Second, we analyzed whether the relationship between the probability of having hypertension and the identified predictor traits was heterogeneous between the biometrically inferred single locus genotypes with large effects on sodium-lithium countertransport level. Third, if there was no heterogeneity, we assessed whether sodium-lithium countertransport genotypes made an additional contribution to predicting the probability of having hypertension ...
Apolipoprotein CIII (apoCIII) is an independent risk for coronary heart disease (CHD). In this study, we investigated the associations among plasma apoCIII, hs-CRP and TNF-α levels and their roles in the clinical features of CHD in the Li and Han ethnic groups in China. A cohort of 474 participants was recruited (238 atherosclerotic patients and 236 healthy controls) from the Li and Han ethnic groups. Blood samples were obtained to evaluate apoCIII, TNF-α, hs-CRP and lipid profiles. Chi-squared, t-tests, and Kruskal-Wallis or Wilcoxon-Mann-Whitney tests, Pearson or Spearman correlation tests and multiple unconditional logistic regression were employed to analyze lipid profiles and variations in plasma apoCIII, TNF-α, hs-CRP in subgroups of CHD and their contributions to CHD using SPSS version 20.0 software. Compared to healthy participants, unfavorable lipid profiles were identified in CHD patients with enhanced systolic pressure, diastolic pressure, fasting blood sugar (FBS), TG, TC, LDL-C, apoB, Lp
OSAKA, Japan and FLORHAM PARK, N.J. and STAMFORD, Conn., March 23, 2017 /PRNewswire/ - Shionogi Inc. and Purdue Pharma L.P. announced today that the U.S. Food and Drug Administration (FDA) approved Symproic® (naldemedine) 0.2 mg tablets C-II as a…. .rlw-block ul{ list-style: none !important; margin-left: 0 !important; padding-left: 0 !important; } .rlw-block .rlw-li { list-style-type: none; } .rlw-block a { display: inline !important; text-decoration: none; font-weight: normal; } .rlw-block h4 { background: none !important; } .rlw-block .rlw-thumb { border: 1px solid #eee !important; box-shadow: none !important; margin: 2px 10px 2px 0; padding: 3px !important; width: 100%; height: 150px; object-fit: cover; } .rlw-summary { font-size: 12px; } .rlw-time { color: #bbb; font-size: 11px; } .rlw-comment { color: #bbb; font-size: 11px; padding-left: 5px; } .rlw-alignleft { display: inline; float: left; } .rlw-alignright { display: inline; float: right; } .rlw-aligncenter { display: block; ...
购买Abcam重组人Lipoprotein lipase (ab115500),经WB验证。全长蛋白。提供28,000多种信号蛋白、细胞因子、趋化因子、生长因子等产品。
Explore the structures and analogues of N-{1-[2-(4-Iodo-2,5-dimethoxyphenyl)ethyl]piperidin-4-yl}-N-phenylpropanamide, N-(2C-I) fentanyl in book II of TiHKAL: The Continuation. Alexander & Ann Shulgin
ApoC-II was the only apolipoprotein from human very low density lipoprotein that activated rat adipose tissue lipoprotein lipase. Activation was blocked by antiserum against apoC-II. Addition of increasing amounts of activator did not alter the apparent Km of lipoprotein lipase (0.32 mM triolein), but it did produce a progressive increase in the apparent Vmax from 0.8 to 2.2 µmoles free fatty acid/mg hour-1. Substrate concentrations above 1.27 mM triolein diminished activation by 0.25-5.0 µg/ml of apoC-II as much as 20%. Reversal of this apparent substrate inhibition was achieved by increasing the activator concentration to 50.0 µg/ml. Each of five nonactivating apolipoproteins-apoC-I, C-III-1, C-III-2, A-I, and A-II-inhibited lipoprotein lipase up to 85-100%. ApoC-II also produced less inhibition under appropriate conditions. Inhibition was dependent on apoprotein concentration, inversely related to substrate triglyceride concentration, and unobserved with nonlipoprotein proteins. The ...
Site-directed mutagenesis and other molecular biology-based techniques are now available for probing the amphipathic alpha-helix structural motif in the exchangeable apolipoproteins. Here we survey the published literature on lipid-binding and functional domains in apolipoproteins A-I, A-II, A-IV, C-I, C-II, C-III, and E and compare these results with recently developed computer methods for analysis of the location and properties of amphipathic helixes. This comparison suggests that there are at least three distinct classes of amphipathic helixes (classes A, Y, and G*) in the exchangeable apolipoproteins whose distribution varies within and between the seven apolipoproteins. This comparison further suggests that lipid affinity resides largely in class A amphipathic helixes (Segrest, J. P., et al. 1990. Proteins. 8: 103) and that variations in structure and/or numbers of class A domains in individual apolipoproteins allow a range of lipid affinities from high to low. The positions of the four a ...
A 39-year-old man with lipoprotein lipase (LPL) deficiency (height 177.7 cm, body weight 67 kg, and body mass index 21.2 kg/m,sup,2,/sup,) showed severe hypertriglyceridemia (2, 032 mg/dl). LPL activity and concentration were markedly low in postheparin plasma. LPL gene analysis revealed a homozygous mutation, Asp204 → Glu in exon 5. Fasting plasma glucose (81 mg/dl) and insulin (2.7 (μU/ml) levels were normal. Plasma glucose pattern during oral glucose (75 g) tolerance test was normal, however 30 minutes after glucose-loading the insulin secretion unexpectedly increased to 89.4 μU/ml. These data suggested that chylomicronemia might be related to a hyper-response of insulin secretion to glucose without obesity.,br,(Internal Medicine 41: 300-303, 2002). ...
Tsao YK, Wei CF, Robberson DL, Gotto AM, Chan L (Dec 1985). "Isolation and characterization of the human apolipoprotein A-II gene. Electron microscopic analysis of RNA:DNA hybrids, nucleotide sequence, identification of a polymorphic MspI site, and general structural organization of apolipoprotein genes". The Journal of Biological Chemistry. 260 (28): 15222-31. PMID 2415515 ...
ProSpecs Apolipoproteins include: Clusterin Human Recombinant, Clusterin Rat Recombinant, Apolipoprotein-D Human Recombinant, Human Apolipoprotein-J, Apolipoprotein-J Canine Recombinant
Apolipoprotein F山羊多克隆抗体(ab81908)可与人样本反应并经WB, ELISA, ICC实验严格验证。所有产品均提供质保服务,中国75%以上现货。
Thank you for your interest in spreading the word about Biochemical Society Transactions.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
View Ldlr/Ldlr Tg(APOC3)3707Bres/? involves: 129S7/SvEvBrd * C57BL/6J * CBA/J: phenotypes, images, diseases, and references.
Retinyl esters (present in meats) and beta-carotene (present in plants) are the two main sources of retinoids in the diet. ... apolipoprotein D; beta-lactoglobulin; complement component C8 gamma chain; crustacyanin; epididymal-retinoic acid binding ... In the event that two species names have identical designations, they are discriminated from one another by adding one or more ... share only one or two of these. Proteins known to belong to this family include alpha-1-microglobulin (protein HC); major ...
Apolipoprotein E (ApoE) plays an important role in phospholipid and cholesterol homeostasis. After binding ApoER2, ApoE is ... Upon reelin binding, Dab1 is phosphorylated by two tyrosine kinases, Fyn and Src. The phosphorylated Dab1 then causes further ... Riddell DR, Sun XM, Stannard AK, Soutar AK, Owen JS (2001). "Localization of apolipoprotein E receptor 2 to caveolae in the ... Herz J (June 2009). "Apolipoprotein E receptors in the nervous system". Curr. Opin. Lipidol. 20 (3): 190-6. doi:10.1097/MOL. ...
Apolipoprotein A-II is a protein that in humans is encoded by the APOA2 gene. This gene encodes apolipoprotein (apo-) A-II, ... Brewer HB, Lux SE, Ronan R, John KM (May 1972). "Amino acid sequence of human apoLp-Gln-II (apoA-II), an apolipoprotein ... Lackner KJ, Law SW, Brewer HB (Sep 1984). "Human apolipoprotein A-II: complete nucleic acid sequence of preproapo A-II". FEBS ... "Entrez Gene: APOA2 apolipoprotein A-II". Pussinen PJ, Jauhiainen M, Metso J, Pyle LE, Marcel YL, Fidge NH, Ehnholm C (Jan 1998 ...
Apolipoprotein L2 is a protein that in humans is encoded by the APOL2 gene. This gene is a member of the apolipoprotein L gene ... Two transcript variants encoding the same protein have been found for this gene. GRCh38: Ensembl release 89: ENSG00000128335 - ... "Entrez Gene: APOL2 apolipoprotein L, 2". Human APOL2 genome location and APOL2 gene details page in the UCSC Genome Browser. ... McGhee KA, Morris DW, Schwaiger S (2005). "Investigation of the apolipoprotein-L (APOL) gene family and schizophrenia using a ...
Apolipoprotein L6 is a protein that in humans is encoded by the APOL6 gene. This gene is a member of the apolipoprotein L gene ... Bonaldo MF, Lennon G, Soares MB (1997). "Normalization and subtraction: two approaches to facilitate gene discovery". Genome ... "Entrez Gene: APOL6 apolipoprotein L, 6". Human APOL6 genome location and APOL6 gene details page in the UCSC Genome Browser. ... Liu Z, Lu H, Jiang Z, Pastuszyn A, Hu CA (Jan 2005). "Apolipoprotein l6, a novel proapoptotic Bcl-2 homology 3-only protein, ...
Apolipoprotein M is a protein that in humans is encoded by the APOM gene. The protein encoded by this gene is an apolipoprotein ... Two transcript variants encoding two different isoforms have been found for this gene, but only one of them has been fully ... "Entrez Gene: APOM apolipoprotein M". Albertella MR, Jones H, Thomson W, et al. (1997). "Localization of eight additional genes ... 2004). "Regulation of apolipoprotein M gene expression by MODY3 gene hepatocyte nuclear factor-1alpha: haploinsufficiency is ...
Zannis VI, Kan HY, Kritis A, Zanni E, Kardassis D (Mar 2001). "Transcriptional regulation of the human apolipoprotein genes". ... two mechanisms for repression". Molecular and Cellular Biology. 20 (1): 187-95. doi:10.1128/MCB.20.1.187-195.2000. PMC 85074 . ... Ginsburg GS, Ozer J, Karathanasis SK (Jul 1995). "Intestinal apolipoprotein AI gene transcription is regulated by multiple ... "Cloning and sequencing of cDNAs encoding the human hepatocyte nuclear factor 4 indicate the presence of two isoforms in human ...
... and apolipoprotein E receptor-2 (ApoER2; 602600), are also required. Both receptors bound Dab1 on their cytoplasmic tails and ... "Functional dissection of Reelin signaling by site-directed disruption of Disabled-1 adaptor binding to apolipoprotein E ... 19 (2): 239-49. doi:10.1016/S0896-6273(00)80936-8. PMID 9292716. Long H, Bock HH, Lei T, Chai X, Yuan J, Herz J, Frotscher M, ... 47 (2): 165-74. doi:10.1002/gcc.20519. PMID 18008369. Deguchi K, Inoue K, Avila WE, et al. (2003). "Reelin and disabled-1 ...
Thus one extra sialyl residue on apolipoprotein C3 impairs its action on lipoprotein lipase. This can affect expression of the ... Galton, DJ (August 2017). "Clarifying complex inheritance: apolipoprotein C3 and atherosclerosis". Current Opinion in ... "An abnormal triglyceride-rich lipoprotein containing excess sialylated apolipoprotein". Journal of Clinical Investigation. 69: ... "Hypertriglyceridaemia associated with an abnormal triglyceride-rich lipoprotein carrying excess apolipoprotein". Lancet. 2: 667 ...
RNA polymerase II regulatory region sequence-specific DNA binding. • RNA polymerase II transcription factor activity, ligand- ... "Farnesoid X receptor agonists suppress hepatic apolipoprotein CIII expression". Gastroenterology. 125 (2): 544-55. doi:10.1016/ ... RNA polymerase II distal enhancer sequence-specific DNA binding. • sequence-specific DNA binding. • DNA binding. • ... RNA polymerase II transcription factor activity, sequence-specific DNA binding. Cellular component. • nuclear euchromatin. • ...
Two transcription initiation sites and two polyadenylation sites are identified in the gene structure. The reelin protein ... All members of this family are receptors for Apolipoprotein E (ApoE). Therefore, they are often synonymously referred to as ' ... Moreover, the two main receptors of reelin are able to form clusters that most probably play a major role in the signaling, ... The two main reelin receptors seem to have slightly different roles: VLDLR conducts the stop signal, while ApoER2 is essential ...
Kim SY, Park SM, Lee ST (January 2006). "Apolipoprotein C-II is a novel substrate for matrix metalloproteinases". Biochem. ... Two molecules of ApoC-II can attach to each LPL dimer. It is estimated that up to forty LPL dimers may act simultaneously on a ... In the Golgi apparatus, the oligosaccharides are further altered to result in either two complex chains, or two complex and one ... "Activation of lipoprotein lipase by native and synthetic fragments of human plasma apolipoprotein C-II". Proc. Natl. Acad. Sci ...
"Two proteins essential for apolipoprotein B mRNA editing are expressed from a single gene through alternative splicing". J. ... Mammalian apolipoprotein B mRNA undergoes site-specific C to U deamination, which is mediated by a multi-component enzyme ... Lau PP, Chang BH, Chan L (April 2001). "Two-hybrid cloning identifies an RNA-binding protein, GRY-RBP, as a component of apobec ... Lau PP, Chang BH, Chan L (2001). "Two-hybrid cloning identifies an RNA-binding protein, GRY-RBP, as a component of apobec-1 ...
"Familial type I hyperlipoproteinemia caused by apolipoprotein C-II deficiency". Atherosclerosis. 34 (1): 53-65. doi:10.1016/ ... Hyperlipoproteinemia type II, by far the most common form, is further classified into types IIa and IIb, depending mainly on ... The lipoprotein density and type of apolipoproteins it contains determines the fate of the particle and its influence on ... For treatment of type II, dietary modification is the initial approach, but many patients require treatment with statins (HMG- ...
Apolipoprotein B48 on chylomicra and Apolipoprotein B100 on LDL, IDL, and VLDL are important for MTP binding. Click on genes, ... Gordon DA (1997). "Recent advances in elucidating the role of the microsomal triaglyceride transfer protein in apolipoprotein B ... 1999). "A common binding site on the microsomal triaglyceride transfer protein for apolipoprotein B and protein disulfide ... The network of endoplasmic reticulum-resident chaperones (ERp72, GRP94, calreticulin, and BiP) interacts with apolipoprotein b ...
... to apolipoproteins A-I and A-II: location of a PLTP binding domain in the amino terminal region of apoA-I". J. Lipid Res. 39 (1 ... to apolipoproteins A-I and A-II: location of a PLTP binding domain in the amino terminal region of apoA-I". J. Lipid Res. 39 (1 ... At least two transcript variants encoding different isoforms have been found for this gene. PLTP has been shown to interact ... The protein encoded by this gene is one of at least two lipid transfer proteins found in human plasma. The encoded protein ...
August 1992). "Apolipoprotein AI mutation Arg-60 causes autosomal dominant amyloidosis". Proc. Natl. Acad. Sci. U.S.A. 89 (16 ... with congenital mutations in apolipoprotein A1 and lysozyme. It is also known as "Ostertag" type, after B. Ostertag, who ... 118 (3): 321-2. doi:10.1016/j.amjmed.2004.10.022. PMID 15745733. Granel B, Valleix S, Serratrice J, et al. (January 2006). " ... 20 (2): 444-51. doi:10.1681/ASN.2008060614. PMC 2637055 . PMID 19073821. Uemichi T, Liepnieks JJ, Gertz MA, Benson MD ( ...
... has been shown to interact with Apolipoprotein A1 and APOA4. GRCh38: Ensembl release 89: ENSG00000112293 - Ensembl, May ... Deeg MA, Bowen RF (2002). "Phosphorylation decreases trypsin activation and apolipoprotein al binding to ... 26 (2): 95-7. PMID 12536633. Mungall AJ, Palmer SA, Sims SK, et al. (2003). "The DNA sequence and analysis of human chromosome ... 53 (2): 138-9. doi:10.1016/j.metabol.2003.09.004. PMID 14767861. Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The Status ...
Apolipoprotein B can exist in two forms: B-100 and B-48. Apoliporotein B-100 is present on several lipoproteins, including very ... Olofsson SO, Boren J (2005). "Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins ... Apolipoprotein B-100 has been linked to the development of atherosclerosis. APOB ( see native LDL-ApoB structure at 37°C on ... Vitellinogen precursors are multi-domain apolipoproteins that are cleaved into distinct yolk proteins. Different vitellinogen ...
... and involves apolipoprotein A1. "FAP-IV" is also known as "Finnish-type", and involves gelsolin. Fibrinogen, apolipoprotein A1 ... Currently there are two ongoing clinical trials undergoing recruitment in the United States and worldwide to evaluate ... "FAP-I" and "FAP-II" are associated with transthyretin. (Senile systemic amyloidosis [abbreviated "SSA"] is also associated with ... These proteins include: transthyretin (ATTR, the most commonly implicated protein), apolipoprotein A1, and gelsolin. Due to the ...
"Entrez Gene: APOBEC3B apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3B". Human APOBEC3B genome location and ... 2 (9): E275. doi:10.1371/journal.pbio.0020275. PMC 479043 . PMID 15269786. Yu Q, Chen D, König R, et al. (2005). "APOBEC3B and ...
"Entrez Gene: APOBEC2 apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 2". Human APOBEC2 genome location and ... 1997). "Tissue-specific inhibition of apolipoprotein B mRNA editing in the liver by adenovirus-mediated transfer of a dominant ... 1994). "Dimeric structure of a human apolipoprotein B mRNA editing protein and cloning and chromosomal localization of its gene ... 200 (1-2): 149-56. doi:10.1016/S0378-1119(97)00411-3. PMID 9373149. Anant S, Mukhopadhyay D, Sankaranand V, et al. (2001). " ...
Amrine-madsen, H.; Koepfli, K.P.; Wayne, R.K.; Springer, M.S. (2003). "A new phylogenetic marker, apolipoprotein B, provides ... 28 (2): 225-240. doi:10.1016/S1055-7903(03)00118-0. PMID 12878460. Retrieved 2008-04-19. Beck, Robin MD; Bininda-Emonds, Olaf ...
This condition is caused by a mutation in apolipoprotein E (ApoE), that serves as a ligand for the liver receptors for ... Primary hyperlipoproteinemia Apolipoprotein B deficiency List of cutaneous conditions Rapini, Ronald P.; Bolognia, Jean L.; ... Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 1-4160-2999-0. James, William D.; Berger, Timothy ...
Apolipoprotein B can exist in two forms: B-100 and B-48. Apolipoprotein B-100 is present on several lipoproteins, including ... Olofsson SO, Borèn J (November 2005). "Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic ... II. Roles of juvenile hormones in adult insects". Advances in Insect Physiology. 26: 1-155. doi:10.1016/S0065-2806(08)60030-2. ... Apolipoprotein B-100 has been linked to the development of atherosclerosis. Honey bees deposit vitellogenin molecules in fat ...
2002). "Regulated expression of the apolipoprotein E/C-I/C-IV/C-II gene cluster in murine and human macrophages. A critical ... Apolipoprotein C-IV, also known as apolipoprotein C4, is a protein that in humans is encoded by the APOC4 gene.[5][6] ... Apolipoprotein (apo)C4 gene is a member of the apolipoprotein C gene family. It is expressed in the liver and has a predicted ... in the apolipoprotein E, C-I, and C-II gene locus". Genomics. 28 (2): 291-300. doi:10.1006/geno.1995.1144. PMID 8530039.. ...
One striking example is the remarkable ability of human apolipoprotein C-II amyloid fibrils to circularize and form closed ... Our results suggest a model for apoC-II fibrils as ribbons approximately 2.1-nm thick and 13-nm wide with a helical repeat ... We use these observed biophysical properties to model the apoC-II amyloid fibrils either as wormlike chains or using a random- ... More generally, the ability of apoC-II fibrils to form rings also highlights the degree to which the common cross-beta ...
Lipid-free human apolipoprotein C-II (apoC-II) forms characteristic amyloid fibrils and is one of several apolipoproteins that ... A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations ... A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations. ... Our structural model for apoC-II fibrils suggests that apoC-II monomers fold and self-assemble to form a stable cross-beta- ...
Distribution of apolipoprotein C-II mRNA and protein in the perinatal mouse lung. Mouse tissue sections are from saccular stage ... Recently, we showed expression of apolipoprotein C-II (apoC-II), the essential cofactor of lipoprotein lipase (LPL), in the ... Recently, we showed expression of apolipoprotein C-II (apoC-II), the essential cofactor of lipoprotein lipase (LPL), in the ... Apolipoprotein C-II and lipoprotein lipase show a temporal and geographic correlation with surfactant lipid synthesis in ...
"Entrez Gene: APOD apolipoprotein D". Muffat J, Walker DW (2010). "Apolipoprotein D: an overview of its role in aging and age- ... Apolipoprotein D (Apo-D) is a component of high-density lipoprotein that has no marked similarity to other apolipoprotein ... Apolipoproteins D at the US National Library of Medicine Medical Subject Headings (MeSH) Applied Research on Apolipoproteins ... Apolipoprotein D is a protein that in humans is encoded by the APOD gene. Unlike other lipoproteins, which are mainly produced ...
... Rampratap S. ... We used 2 cynomolgus monkeys and 3 baboons fed a cholesterol- and fat-enriched diet. In cynomolgus monkeys, we injected ... 2BioNumerik Pharmaceuticals, Inc, San Antonio 78229, TX, USA. Received 24 November 2003; Revised 26 May 2004; Accepted 2 June ... Kushwaha,1 Henry C. McGill,1 and Frederick H. Hausheer2 1Department of Physiology and Medicine, Southwest Foundation for ...
Apolipoprotein C-II deficiency (APOC2) Test Cost INR 30000.00 Surat Pune Jaipur Lucknow Kanpur Nagpur Visakhapatnam Indore ... Apolipoprotein C-II deficiency (APOC2) Test Description. Apolipoprotein C-II deficiency (APOC2) Apolipoprotein C-II deficiency ... Apolipoprotein C-II deficiency (APOC2) TEST DETAILS. Deatils about the test Apolipoprotein C-II deficiency (APOC2). *What is ... Make the payment Online for Apolipoprotein C-II deficiency (APOC2). * Fill the Form with your details for Apolipoprotein C-II ...
Literature: Apolipoprotein A-II (ApoA-II) (IPR006801). References used in this entry. The following publications were referred ... Structures of apolipoprotein A-II and a lipid-surrogate complex provide insights into apolipoprotein-lipid interactions.. Kumar ... Apolipoprotein A-II, HDL metabolism and atherosclerosis.. Tailleux A, Duriez P, Fruchart JC, Clavey V.. Atherosclerosis 164 1- ... Purification, primary structure, and antimicrobial activities of bovine apolipoprotein A-II.. Motizuki M, Itoh T, Yamada M, ...
Anti-Apolipoprotein A II antibody conjugated to Biotin validated for WB, ELISA and tested in Human. Immunogen corresponding to ... Anti-Apolipoprotein A II antibody (Biotin). See all Apolipoprotein A II primary antibodies. ... The antibody can be used for detection of human Apolipoprotein A II in plasma and lipoproteins, immunoassays and immunoblots. ... Shipped at 4°C. Store at +4°C short term (1-2 weeks). Store at -20°C or -80°C. Avoid freeze / thaw cycle. ...
Sheep polyclonal Apolipoprotein A II antibody validated for WB, ELISA and tested in Human. Immunogen corresponding to full ... Anti-Apolipoprotein A II antibody. See all Apolipoprotein A II primary antibodies. ... Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. ...
Anti-Apolipoprotein A II antibody conjugated to HRP validated for WB, ELISA and tested in Human. Immunogen corresponding to ... Anti-Apolipoprotein A II antibody (HRP). See all Apolipoprotein A II primary antibodies. ...
Rabbit recombinant monoclonal Apolipoprotein A II antibody [EPR2913] validated for WB, Flow Cyt, ICC/IF and tested in Human and ... Anti-Apolipoprotein A II antibody [EPR2913]. See all Apolipoprotein A II primary antibodies. ... Anti-Apolipoprotein A II antibody [EPR2913] (ab92478) at 1/1000 dilution + Human plasma. lysate at 10 µg. Secondary. HRP ... Immunocytochemistry/ Immunofluorescence - Anti-Apolipoprotein A II antibody [EPR2913] (ab92478)This image is courtesy of an ...
Goat polyclonal Apolipoprotein A II antibody validated for WB, IP, ELISA, IHC and tested in Human. Immunogen corresponding to ... Anti-Apolipoprotein A II antibody. See all Apolipoprotein A II primary antibodies. ... This antibody recognises Human Apolipoprotein A II. Exhibits very low cross reactivity with Type A I, B, C I, C II, C III, E ... Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Apolipoprotein A II antibody (ab85749) ...
Structure of a biologically active fragment of human serum apolipoprotein C-II in the presence of sodium dodecyl sulfate and ... APOLIPOPROTEIN C-II A 36 Homo sapiens Fragment: RESIDUES 44-79 Gene Name(s): APOC2 Gene View APC2 Gene View ... RCSB PDB (citation) is managed by two members of the Research Collaboratory for Structural Bioinformatics: Rutgers and UCSD/ ...
References for Abcams Anti-Apolipoprotein A II antibody (HRP) (ab20825). Please let us know if you have used this product in ...
Absence of CC chemokine receptor-2 reduces atherosclerosis in apolipoprotein E-deficient mice.. Dawson TC1, Kuziel WA, Osahar ...
Structure of a biologically active fragment of human serum apolipoprotein C-II in the presence of sodium dodecyl sulfate and ... RCSB PDB (citation) is managed by two members of the Research Collaboratory for Structural Bioinformatics: Rutgers and UCSD/ ... ACTION - (A) Select for download / view details OR (B) Select two chains for comparison ... You can also use the structure comparison tool to compare any 2 given structures. ...
Anti-Apolipoprotein A II antibody conjugated to FITC validated for ICC/IF and tested in Human. Immunogen corresponding to full ... Anti-Apolipoprotein A II antibody (FITC). See all Apolipoprotein A II primary antibodies. ...
Browse our Apolipoprotein A-II/ApoA2 Antibody catalog backed by our Guarantee+. ... Apolipoprotein A-II/ApoA2 Antibodies available through Novus Biologicals. ... anti-apolipoprotein A-II antibody, anti-Apolipoprotein A2 antibody. 6 Results for "apolipoprotein-a-ii-apoa2" in Primary ... Alternate Names for Apolipoprotein A-II/ApoA2 Antibodies. anti-Apolipoprotein A-II/ApoA2 antibody, anti-APOA2 antibody, anti- ...
Browse our Apolipoprotein A-II/ApoA2 Antibody catalog backed by our Guarantee+. ... Apolipoprotein A-II/ApoA2 Antibodies available through Novus Biologicals. ... Alternate Names for Apolipoprotein A-II/ApoA2 Antibodies. anti-Apolipoprotein A-II/ApoA2 antibody, anti-APOA2 antibody, anti- ... Apolipoprotein A-II/ApoA2 Antibodies. We offer Apolipoprotein A-II/ApoA2 Antibodies for use in common research applications: ...
Y. Zhao, Z. Guo, X. Lin et al., "Apolipoprotein E-deficient lipoproteins induce foam cell formation by activation of PERK-EIF-2 ... J. A. Piedrahita, S. H. Zhang, J. R. Hagaman, P. M. Oliver, and N. Maeda, "Generation of mice carrying a mutant apolipoprotein ... A. H. Hasty, M. F. Linton, L. L. Swift, and S. Fazio, "Determination of the lower threshold of apolipoprotein E resulting in ... D. Wu, C. Sharan, H. Yang et al., "Apolipoprotein E-deficient lipoproteins induce foam cell formation by downregulation of ...
Lipoprotein(a), Apolipoprotein(a) Polymorphism, and Insulin Treatment in Type II Diabetic Patients. ... Lipoprotein(a), Apolipoprotein(a) Polymorphism, and Insulin Treatment in Type II Diabetic Patients ... Lipoprotein(a), Apolipoprotein(a) Polymorphism, and Insulin Treatment in Type II Diabetic Patients ... Lipoprotein(a), Apolipoprotein(a) Polymorphism, and Insulin Treatment in Type II Diabetic Patients ...
Selected quality suppliers for anti-Apolipoprotein C-II antibodies. ... Order monoclonal and polyclonal Apolipoprotein C-II antibodies for many applications. ... More Antibodies against Apolipoprotein C-II Interaction Partners. Zebrafish Apolipoprotein C-II (APOC2) interaction partners ... Additionally we are shipping Apolipoprotein C-II Kits (51) and Apolipoprotein C-II Proteins (28) and many more products for ...
Apolipoprotein E Polymorphism and Renal Function in German Type 1 and Type 2 Diabetic Patients. ... Apolipoprotein E Polymorphism and Renal Function in German Type 1 and Type 2 Diabetic Patients ... Apolipoprotein E Polymorphism and Renal Function in German Type 1 and Type 2 Diabetic Patients ... Apolipoprotein E Polymorphism and Renal Function in German Type 1 and Type 2 Diabetic Patients ...
Apolipoprotein A-II (A-II) did not increase with age in men (r = −0.20, n = 172), but showed a slight increase with age in ... To study apolipoprotein A-II, a simple, precise, and accurate immunodiffusion assay was developed and applied in a population ... The Measurement of Apolipoprotein A-I and A-II Levels in Men and Women by Immunoassay. ... The Measurement of Apolipoprotein A-I and A-II Levels in Men and Women by Immunoassay. ...
OBJECTIVE: Apolipoprotein(B) [apo(B)] reflects the total mass of atherogenic particles (VLDL, IDL, and LDL), and its increase ... Apolipoprotein(B) identifies dyslipidemic phenotypes associated with cardiovascular risk in normocholesterolemic type 2 ... Apolipoprotein(B) identifies dyslipidemic phenotypes associated with cardiovascular risk in normocholesterolemic type 2 ... Apolipoprotein(B) identifies dyslipidemic phenotypes associated with cardiovascular risk in normocholesterolemic type 2 ...
  • The major sites of apoC-II and LPL gene expression changed over time and were found mainly in the distal epithelium at the end of gestation but not after birth. (nih.gov)
  • The major site of apoC-II mRNA synthesis (positive signal, blue) changed after birth (compare A to C). Positive signals were found in newly-formed septa (D, E) and macrophages (E) on PN 5. (nih.gov)
  • Immunohistochemistry (below the yellow line) (G-O) was performed using an anti-apoC-II polyclonal antibody (G to I, K to M, O) or goat IgG as negative control (J, N). Positive signals (red) were found in secretory granule-like structures in distal epithelial cells on GD 19.5 (H) and PN0 (G) but not in later timepoints. (nih.gov)
more