TY - JOUR. T1 - Genetic control of apolipoprotein A-I distribution among HDL subclasses. AU - Rainwater, David L.. AU - Blangero, John. AU - Moore, Perry H.. AU - Shelledy, Wendy R.. AU - Dyer, Thomas D.. PY - 1995. Y1 - 1995. N2 - We conducted genetic analyses to determine the components of variation for size distributions of apolipoprotein (apo) A-I among human plasma lipoproteins resolved on the basis of size. Analyses used data for 717 individuals in 26 pedigrees. Apo A-I distributions among lipoprotein size classes were measured by nondenaturing gradient gel electrophoresis (GGE) and immunoblotting procedures. Curves were fitted to apo A-I absorbance profiles to estimate fractional absorbance in each of five high-density lipoprotein (HDL) subclasses. Multivariate regression analyses revealed several covariates (sex, age, diabetes, and apo A-I concentrations) that were significantly associated with variation in one or more HDL subclasses. Female gender and elevated apo A-I concentrations ...
Carballo-Jane, Ester ; Chen, Zhu ; Oneill, Edward ; Wang, Jun ; Burton, Charlotte ; Chang, Ching H ; Chen, Xun ; Eveland, Suzanne ; Frantz-Wattley, Betsy ; Gagen, Karen ; Hubbard, Brian ; Ichetovkin, Marina ; Luell, Silvi ; Meurer, Roger ; Song, Xuelei ; Strack, Alison ; Langella, Annunziata ; Cianetti, Simona ; Rech, ...
The expression of the apolipoprotein A-I (apo A-I) gene was investigated in the myelinating sciatic nerve. Hybridization analysis with an apo A-I cDNA probe obtained from a cDNA library of mRNA isolated from rapidly myelinating chick sciatic nerve indicated that apo A-I coding transcripts increase during development in the chick sciatic nerve in parallel with the increase of myelin lamellae. Substantial apo A-I-like immunoreactivity in chick sciatic nerve homogenates was detected by Western blotting. The amount of antigen increased from the 15-d embryonic stage to 1 d posthatch and then decreased. Two subcellular fractions corresponding to the cytoplasmic compartments were particularly enriched in apo A-I. apo A-I immunoreactivity was also found in highly purified myelin preparations. Immunohistochemical staining provided further evidence for the presence of apo A-I in the endoneurial compartment of the sciatic nerve. Electron microscopic examination of these fractions after negative staining ...
Because of the inverse relationship between HDL and apo A-I levels and the risk of coronary heart disease in the general population, factors that regulate and, in particular, increase plasma levels of these parameters are of great interest for their potential health benefits. It has been projected that for each 0.026-mmol/L increase in HDL cholesterol levels, the risk of coronary heart disease decreases by 2% to 3%.32 Estrogen has clearly been shown to fall in the category of HDL cholesterol-raising drugs. However, clinical studies have shown that the route of administration of estrogen influences its effects on HDL cholesterol levels. It has been shown that transdermal administration of estrogen does not significantly increase HDL cholesterol levels in postmenopausal women, even though serum estradiol levels in these women are raised to premenopausal levels.13 Oral administration of estrogen results in a 15% to 36% increase in HDL cholesterol levels.12 13 This suggests that exposure of hepatic ...
Endothelial lipase (EL) is a recently discovered member of the lipoprotein lipase gene family that hydrolyzes HDL phospholipids ex vivo and reduces HDL cholesterol (HDL-C) levels when overexpressed in vivo in mice. To gain further insight into the physiological role of EL in the metabolism of HDL in vivo, studies were performed in which EL was inhibited in wild-type, hepatic lipase knockout (HL-/-), and human apoA-I transgenic mice by intravenous infusion of a polyclonal antibody inhibitory to murine EL. As compared with infusion of a control antibody, infusion of the inhibitory antibody resulted in a 25-60% increase in HDL-C levels in the three mouse models, with the peak HDL-C levels occurring at 48 hours after injection. Inhibition of EL also generated larger HDL particles in the HL-/- mice. The clearance of HDL phospholipid was significantly slower in human apoA-I transgenic mice injected with an antibody against murine EL (mEL) than in mice injected with a control antibody. We conclude that ...
RVX-208 (CAS: 1044870-39-4) is a small molecule that increases apolipoprotein A-I and high-density lipoprotein cholesterol in vitro and in vivo; is a BET bromodomain antagonist. RVX-208 may be a promising new approach to the treatment of atherosclerosis.
Objective: D-4F, an apolipoprotein A-I (apoA-I) mimetic peptide, exerts a variety of atheroprotective functions similar to apoA-I, the major protein component of high density lipoprotein (HDL), including acting as an antioxidant, mediating cholesterol efflux from foam cells and direct anti-inflammatory effects. Our previous studies have demonstrated that endoplasmic reticulum (ER) stress promotes macrophage-derived foam cell formation by upregulating CD36 expression and mediates oxidized low-density lipoprotein (ox-LDL)-induced macrophage apoptosis. The goal of this study was to investigate the protective effect of D-4F on ox-LDL-induced macrophage cytotoxicity and specifically the ER stress-C/EBP homologous protein (CHOP) pathway-mediated apoptosis.. Methods and Results: Treatment with D-4F (12.5, 25 and 50 mg/L) attenuated ox-LDL (100 mg/L)-induced cholesterol accumulation in RAW264.7 macrophages and foam cell formation in a dose-dependent manner. Similar to tunicamycin (TM), a classical ER ...
Low-density lipoprotein is recognized as a primary vascular risk factor. However, recent data favor apolipoprotein (apo)B and apoA-I as risk factors with higher predictive values than conventional lipids. We investigated how leisure-time physical activity relates to the serum apoB/apoA-I ratio in...
Apolipoprotein A-I (apo A-I) is the most abundant protein in high-density lipoprotein (HDL) particles, and it plays an important role in HDL metabolism. Both apo A-I and HDL cholesterol (HDL-C) levels are inversely associated with risk of cardiovascular disease. Segregation analyses suggest apo A-I levels are under the control of one or more major loci. Since HDL particles are heterogeneous in their composition and size, genetic influence on its subfractions (i.e., HDL2 and HDL3) could vary. A previous report showed evidence of a major locus controlling HDL3-C levels in a subset of the current study population. Because quantitative trait loci involved in complex diseases are likely to have pleiotropic effects on several related traits, it is possible to have a common major gene involved in regulating apo A-I and HDL3-C levels. We performed a bivariate segregation analysis of apo A-I and HDL3-C levels in 1,006 individuals from 137 families ascertained through probands undergoing elective, diagnostic
Considerable attention has focused on the development of new therapeutic agents that substantially elevate levels of HDL-C. However, development of pharmacological therapies that raise HDL-C levels has been challenging, in part because the underlying biology is substantially more complex than other lipoprotein-directed therapies. HDL circulates in many forms, including both lipid-rich and lipid-poor subfractions (12). It appears that lipid-poor preβ1-HDL fractions acquire cholesterol from macrophages in atherosclerotic plaques. These particles increase in size as they accumulate cholesterol. Cholesterol is ultimately taken up by the liver from these larger, lipid-rich α1-HDL particles or transferred to apoB-containing particles, a process known as RCT (13). Preβ1-HDL represents the most efficient substrate for enhancing RCT, which is considered a pivotal mechanism underlying the potential benefits of HDL-C-raising therapies (14). Because apoA-I has the capacity to generate more lipid-poor ...
Human apolipoprotein (apo) A-I is secreted as a proprotein of 249 amino acids and is processed extracellularly to the mature form (243 amino acids) by removal of a six-residue propeptide segment. We have examined the role of the apoA-I propeptide in intracellular transport and secretion using transfected baby hamster kidney cells that secreted either proapoA-I (from the wild-type cDNA, A-Iwt) or mature-form apoA-I (from A-I delta pro, a cDNA in which the propeptide sequence was deleted). Deletion of the propeptide from the apoA-I sequence did not affect the rate of apoA-I synthesis, nor did it affect the fidelity of proteolytic removal of the prepeptide. However, the propeptide deletion caused mature-form apoA-I to accumulate within the cells as determined by pulse-chase experiments; the intracellular retention times for the mature-form apoA-I in which the propeptide was prematurely removed was three times longer than that of proapoA-I (t1/2 , 3 h compared with approximately 50 min). There was ...
TY - JOUR. T1 - Apolipoprotein A-I increases insulin secretion and production from pancreatic β-cells via a G-protein-cAMPPKA-FoxO1-dependent mechanism. AU - Cochran, Blake J.. AU - Bisoendial, Radjesh J.. AU - Hou, Liming. AU - Glaros, Elias N.. AU - Rossy, Jérémie. AU - Thomas, Shane R.. AU - Barter, Philip J.. AU - Rye, Kerry Anne. PY - 2014/10. Y1 - 2014/10. N2 - Objective - Therapeutic interventions that increase plasma levels of high-density lipoproteins and apolipoprotein A-I (apoA-I) A-I, the major high-density lipoprotein apolipoprotein, improve glycemic control in people with type 2 diabetes mellitus. High-density lipoproteins and apoA-I also enhance insulin synthesis and secretion in isolated pancreatic islets and clonal β-cell lines. This study identifies the signaling pathways that mediate these effects.Approach and Results - Incubation with apoA-I increased cAMP accumulation in Ins-1E cells in a concentration-dependent manner. The increase in cAMP levels was inhibited by ...
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Chymase preferentially cleaved apoA-I at different domains in the lipid-free and lipid-bound forms. The lipid-free form was mainly digested at the C-terminus rather than the N-terminus, especially at Phe229 and Tyr192. In contrast, the lipid-bound form (HDL3), with a relatively higher resistance to cleavage, was digested in the N-terminus, especially at Phe33. Considering the three-dimensional structure of lipid-free apoA-I [14], both CCL/MS (chemical cross-linking/MS) [15] and X-ray analysis [16] essentially provide similar insight: lipid-free apoA-I consists of four N-terminal (amino acids 1-187) and 2 C-terminal (amino acids 188-243) α-helix bundles. However, the in-solution conformation obtained by CCL/MS seems to be less organized and more flexible than the crystal structure obtained from the X-ray analysis. The N-terminal domain constructs a stable antiparallel helix-bundle though the formation of a hydrophobic core by all four N-terminal helices. Because aromatic amino acid residues, ...
Apo-A1 is a 29.0 kDa protein produced in the liver and intestine, and secreted as the predominant constituent of nascent high-density lipoprotein (HDL) particle. Apo-A1, which is found exclusively in HDL, has a unique ability to capture and solubilize free cholesterol. This Apo- 1 ability enables HDL to remove excess peripheral cholesterol and return it to the liver for recycling and excretion. This process, called reverse cholesterol transport, is though to inhibit atherogenesis. For this reason HDL is also known as the "good cholesterol." The therapeutic potential of Apo-A1 has been recently assessed in patients with acute coronary syndromes, using a recombinant form of a naturally occurring variant of Apo-A1 (called Apo-A1 Milano). The availability of recombinant normal Apo-A1 should facilitate further investigation into the potential usefulness of apoA-I in preventing atherosclerotic vascular diseases. Recombinant human Apo-A1 is a 28.2 kDa protein of 244 amino acid residues ...
Apolipoprotein A1 antibody [5F4F5] (apolipoprotein A-I) for ELISA, WB. Anti-Apolipoprotein A1 mAb (GTX83043) is tested in Human samples. 100% Ab-Assurance.
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The HDLs are responsible for the removal of free cholesterol from the blood. Low plasma levels of HDL are associated with increased cardiovascular risk. Low levels of HDL are frequently seen in patients with insulin resistance, from the metabolic syndrome to overt diabetes mellitus. Badimon et al. (59,60) elegantly demonstrated the antiatherogenic properties of HDL, reducing the number of fatty streaks and inducing disease regression in the rabbit experimental model. More recently, Rong et al. (61) evaluated the effects of HDL in advanced experimental atherosclerosis. Diseased thoracic aortic segments from hypercholesterolemic apolipoprotein E-deficient mice were transplanted in the abdominal aorta of apolipoprotein E-deficient mice not expressing (plasma HDL cholesterol approximately 26 mg/dl) or expressing (HDL approximately 64 mg/dl) a human apolipoprotein AI transgene. Mice with high plasma HDL showed significant changes in plaque composition, with macrophage area reductions ,80% and ...
Anti-Apolipoprotein E4 antibody conjugated to Biotin validated for WB, ELISA, RIA and tested in Human. Immunogen corresponding to recombinant full length…
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Diabetic (DM) patients have exacerbated atherosclerosis and high CVD burden. Changes in lipid metabolism, lipoprotein structure, and dysfunctional HDL are characteristics of diabetes. Our aim was to investigate whether serum ApoA-I, the main protein in HDL, was biochemically modified in DM patients. By using proteomic technologies, we have identified a 26 kDa ApoA-I form in serum. MS analysis revealed this 26 kDa form as a novel truncated variant lacking amino acids 1-38, ApoA-IΔ(1-38). DM patients show a 2-fold increase in ApoA-IΔ(1-38) over nondiabetic individuals. ApoA-IΔ(1-38) is found in LDL, but not in VLDL or HDL, with an increase in LDL3 and LDL4 subfractions. To identify candidate mechanisms of ApoA-I truncation, we investigated potentially involved enzymes by in silico data mining, and tested the most probable molecule in an established animal model of diabetes. We have found increased hepatic cathepsin D activity as one of the potential proteases involved in ApoA-I truncation. ...
Carballo-Jane, Ester ; Chen, Zhu ; Oneill, Edward ; Wang, Jun ; Burton, Charlotte ; Chang, Ching H ; Chen, Xun ; Eveland, Suzanne ; Frantz-Wattley, Betsy ; Gagen, Karen ; Hubbard, Brian ; Ichetovkin, Marina ; Luell, Silvi ; Meurer, Roger ; Song, Xuelei ; Strack, Alison ; Langella, Annunziata ; Cianetti, Simona ; Rech, ...
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。
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ヤギ・ポリクローナル抗体 ab7613 交差種: Hu 適用: WB,IP,ELISA…Apolipoprotein A I抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。
ヤギ・ポリクローナル抗体 ab20376 交差種: Ms,Rat 適用: RID…Apolipoprotein A I抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。
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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 ...
Its been six years since I titled a post Remember Apo-A1 Milano? If you go back even further, I wrote about the topic on this blog back in 2003 (!); scroll
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ABCA1 expression and co-localization with [1-93]ApoA-I and ApoA-I. (A) Western blot analysis with anti-ABCA1 antibodies of cell lysates prepared from HepG2 ce
Introduction: Niacin is one of the most potent drugs available to increase high density lipoprotein cholesterol (HDL-C) levels. However the mechanism responsible for the HDL-C increase in response to niacin is not fully understood. We examined the effect of niacin on HDL-C using a humanized mouse model of HDL metabolism, human apoA-I transgenic mice expressing CETP.. Methods and Results: Human apolipoprotein A-I transgenic (hA-I tg) mice (n=18) were transduced with adeno-associated virus (AAV2/8; 1.0 x 1010 gene copies) containing CETP with a liver-specific thyroxine binding globulin (TBG) promoter or control virus. Two weeks following transduction, mice were fed either a chow or chow containing 3% niacin for 2 weeks. Niacin treatment significantly increased HDL-C (34%; p,0.01) in hA-I tg mice expressing CETP. We did not see HDL-C increase in mice injected with control virus following treatment with niacin. Niacin reduced CETP protein mass 78% (p,0.01) and mRNA by 97% (p,0.01) compared to chow ...
Understanding the determinants of HDL function is widely considered a critical priority in HDL research. Given the heterogeneity of HDL species in the circulation, understanding the transporters essential for cholesterol efflux and the HDL species, which are the major contributors to this process may direct contemporary strategies to optimize HDL function or deliver novel HDL analogues in vivo. The present study, which represents the most detailed evaluation of HDL particle size and cellular cholesterol efflux via ABCA1 and ABCG1 to date, has identified HDL size as a key determinant of the efflux capacity of HDL. We further demonstrate that ABCA1 is a quantitatively critical mediator of cholesterol efflux to HDL3, and that HDL3b, HDL3c and lipid-free apoA-I are all suitable therapeutic targets for optimizing cellular cholesterol efflux.. It is a widely held view that ABCA1 is an important mediator of cholesterol export and that it specifically requires apolipoproteins (such as apoA-I) that ...
Background: Type 2 diabetes is a common disease with increased mortality and morbidity due to cardiovascular disease (CVD). This thesis is based on three studies that evaluated traditionally used and emerging risk markers to identify individuals with high-risk of developing CVD in middle-aged men and women with type 2 diabetes. One study was conducted to compare the equivalence between two different ultrasound techniques to measure intima-media thickness since IMT was used to evaluate subclinical atherosclerosis as a surrogate endpoint.. Methods: Data from the cohort study, cardiovascular risk in type 2 diabetes - a prospective study in primary care (CARDIPP) was used in paper I, III and IV. In paper I, baseline data from the first 247 subjects was analysed. Associations between traditionally measured lipids, apolipoproteins, glycaemic control and low-grade inflammation and IMT were analysed.. In paper III, the full baseline cohort, with data from 761 subjects from the CARDIPP study was ...
Effects of Red Grape Juice Consumption on High Density Lipoprotein-Cholesterol, Apolipoprotein AI, Apolipoprotein B and Homocysteine in Healthy Human Volunteers
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 ...
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Background: We evaluated the effects of intravenously administered rAAV8 encoding Apo A-I Milano on aortic and innominate artery atherosclerosis, plaque composition and phenotype of circulating mononuclear cells in Apo E−/− Apo A1−/− mice.. Methods: Mice received one intravenous injection of 1.2x1012 vector genome copies of rAAV8 - Milano or empty vector (12 mice per group). Four weeks after injection mice were placed on high fat diet. Twenty weeks later mice were euthanized and the extend of atherosclerosis in the aorta, aortic sinuses, and innominate artery was measured. Oil-red o staining and Moma-2 staining were used to measure lipid content and macrophage content of the plaques respectively. Quantitative PCR (qPCR) was used to analyze phenotype of macrophages.. Results: Compared to vector control, the Milano recipients had less atherosclerosis in whole aorta (13.4 ± 1.1 % vs. 7.7 ± 0.06%, p= 0.001), in aortic sinuses (77.1 ±9.6 vs 44.8 ±2.3,p=0.01 ) and in the innominate artery ...
In general, transendothelial transport of proteins occurs by paracellular and transcellular pathways. We have previously demonstrated that aortic ECs bind, internalize, and resecrete apoA-I in a competed and temperature-dependent manner.9,10 Furthermore, we demonstrated that ABCA1 but not SR-BI modulates this process.9 In the present study, we extend these findings by showing that ECs also bind, internalize, and transport mature HDL, however, by characteristics that are distinct from those of transendothelial apoA-I transport. Most importantly, SR-BI and ABCG1 but not ABCA1 are rate-limiting for HDL transport.. The presence of different pathways for the transendothelial transport of apoA-I and HDL parallels the need of at least 2 distinct molecules interacting with cells of the arterial wall and other extravascular compartments. Lipid-free apoA-I dissociates from mature HDL as a result of HDL remodeling by lipid transfer proteins and lipases.12-14 Lipid-free apoA-I is important to mediate lipid ...
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。
Evidence-Based Complementary and Alternative Medicine (eCAM) is an international peer-reviewed, Open Access journal that seeks to understand the sources and to encourage rigorous research in this new, yet ancient world of complementary and alternative medicine.
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Because the apparent reduction in cardiovascular risk noted in nondiabetic populations that ingest diets rich in marine lipids containing ω-3 fatty acids is believed to result in part from their capacity to modify the composition and physicochemical behavior of lipoproteins, we sought to determine whether dietary supplementation with marine lipids might favorably affect lipoprotein composition in insulin-dependent diabetes mellitus (IDDM). Eight normolipidemic IDDM women (mean ± SD age 29.8 ± 4.7 yr) were studied before and 3 mo after receiving a marine-lipid concentrate (Super-EPA) containing 6 g ω-3 fatty acids and a total of 12 mg of cholesterol daily. Weight, insulin requirements, and glycosylated hemoglobin remained stable. After treatment, mean ± SD plasma triglyceride (TG) levels fell (before, 81.7 ± 22 mg/dl; after, 69.19 ± 17; P , 0.025). High-density lipoprotein2 (HDL2) cholesterol (before, 10.98 ± 5.45 mg/dl; after, 18.43 ± 7.93; P , 0.01), its major apolipoprotein A-I ...
The effects of the plasma pattern of GH on serum and lipoprotein levels of total cholesterol, triglycerides, apolipoprotein A-I (apo A-I), apolipoprotein B 48/100 (apo B), and apolipoprotein E (apo E) were studied in hypophysectomized female Sprague-
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Epicatechin and cocoa metabolites caused an increase in ApoAI expression in HepG2 cells. Electrophoretic mobility shift assays revealed the involvement of Sites A and B of the ApoAI promoter in the induction of ApoAI mRNA upon incubation with cocoa metabolites. Using supershift assays, we demonstrated the binding of HNF-3β, HNF-4, ER-α, and RXR-α to Site A and the binding of HNF-3β, NFY, and Sp1 to Site B. Luciferase assays performed with a construct containing Site B confirmed its role in the upregulation of ApoAI by cocoa metabolites. Incubation with 3-methyl-epicatechin led to an increase in HNF-3β mRNA, HNF-3β, ER-α, Sp1, and NFY protein levels and the activation of ApoAI transcription mediated by NFY, Sp1, and ER-α. ...
LDL and its major protein, apolipoprotein B, play an essential role in lipid transport and metabolism. Apo B may regulate cholesterol synthesis through its interaction with specific cell membrane receptors and by inhibition of HMG Co A reductase. This enzyme has been identified as the rate controlling enzyme in cholest