|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for APOA1(NM_001318018.2) Search again
Product ID:
HQP149751
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HPALP2, apo(a)
Gene Description:
apolipoprotein A1
Target Gene Accession:
NM_001318018.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes apolipoprotein A-I, which is the major protein component of high density lipoprotein (HDL) in plasma. The protein promotes cholesterol efflux from tissues to the liver for excretion, and it is a cofactor for lecithin cholesterolacyltransferase (LCAT) which is responsible for the formation of most plasma cholesteryl esters. This gene is closely linked with two other apolipoprotein genes on chromosome 11.
Gene References into function
- Apolipoprotein A-I alpha -helices 7 and 8 modulate high density lipoprotein subclass distribution
- translocation of cholesterol and phospholipid into the cytosol is related to the apo A-I-mediated HDL assembly in astrocytes through functional association with caveolin-1 and a cyclosporin A-sensitive cyclophilin protein(s).
- Effects of enrichment of fibroblasts with unesterified cholesterol on the efflux of cellular lipids to apolipoprotein A-I
- significance of G--->A polymorphism in gene promoter on serum high density lipoprotein cholesterol levels in Japanese hyperlipidemic subjects
- Polymorphisms are not associated with severe aortic valve stenosis
- mechanism for the induction of apoA-I might include PPAR-gamma for which oxidized fatty acid is a ligand.
- Infusion of APOA1 into fasting healthy male subjects activated FVII, increased TAT complex blood levels, and decreased HDL triglyceride blood levels.
- Apo AI/ABCA1-dependent and HDL3-mediated lipid efflux
- individual and combined associations of the apolipoprotein (apo) A-I -75 bp and +83 bp polymorphisms with plasma lipid, lipoprotein and apolipoprotein levels in 734 Caucasian men and women
- APOA1 to APOB ratio is related to myocardial infarction and stroke
- Mutations may be associated with hypertension
- In conclusion, 12% of Hypoalphalipoproteinemia subjects were found to carry mutations in apo A-I, LCAT, or GBA genes
- APOA1 has a varying conformational states as it adjusts from a discoidal to a spherical surface
- Observations of the effects of four mutations in the central region of lipid-free apoA-I (residues 123-165) are consistent with the helical structure of residues 145-164 and the disordered structure of residues 123-142 in lipid-free apoA-I.
- structure-function studies of variants
- additive influence of mutant APOA1 and testosterone on plasma HDL-cholesterol
- Pre-beta apoA-I is formed during cholesteryl ester transfer protein-mediated remodeling of reconstituted HDL, a process in which the phospholipid composition of the particles plays a key role.
- apolipoprotein AI conformation required for systemic amyloidosis is described
- apolipoproteins appear to be a class of mediators that can participate in the regulation of the activity of neutrophils
- study of structural and functional homology between human apolipoprotein A-I and envelope proteins of human immunodeficiency virus type 1 in CD4 receptor binding
- APOA1 has a role in regulating ABCA1 expression in macrophages
- Degradation of phospholipid transfer protein (PLTP) and PLTP-generated protein by mast cell chymase impairs high affinity efflux of cholesterol from macrophage foam cells.
- comparison of 5 natural point mutations illustrates that a specific sequence between amino acids 110 and 162 is required for LCAT activation
- Results show that during the early stages, oxidation of HDL gives rise to specifically oxidized forms of apolipoproteins A-I and A-II.
- REVIEW: an update on the experimental studies in which apolipoprotein A-I(Milano), produced as a recombinant protein, has displayed important effects in the treatment of vascular diseases
- Apolipoprotein A-II inhibits high density lipoprotein remodeling and lipid-poor formation of this protein
- Hepatitis B virus (HBV) reduced steady-state levels of apolipoprotein AI mRNAs in two hepatoma cell lines
- the structural organization of lipid-free apoA-I and the role of different domains in lipid binding, with comparisons to apoE
- Individuals with this protein are at a higher risk for schizophrenia.
- The spatial organization of apolipoprotein A-I on the edge of discoidal high density lipoprotein particles: a mass specrometry study.
- In an LDL receptor-deficient mouse model of familial hypercholesterolemia, helper-dependent adenovirus gene transfer of human apoA-I causes long-term overexpression of apoA-I and retards atherosclerosis progression
- EPR spectroscopy was used to examine the structure of the apoA-I C terminus in lipid-free and lipid-associated states.Spectra of apoA-I in reconstituted HDL revealed a lipid-induced transition of defined beta-strands into alpha-helices
- APOAI had distinct inhibitory effects on the lipolysis of large and small emulsions: more effective inhibition for small emulsions.
- HDL cholesterol levels were 4% (0.06 mmol/l) and 10% (0.15 mmol/l) higher in heterozygotes and mutation homozygotes; the equivalent values for apolipoprotein A1 were 3% and 7% higher.
- G/A polymorphism of the apo A-I promoter region affects not only baseline HDL-C concentrations but also its response to pravastatin treatment.
- Apo A-I mutations cannot be firmly establihed in samll number of patients with severe HDL deficiency.
- APOA1 has a role in formation of nascent high density lipoprotein particles
- apoA-I activates PKC alpha by PC-PLC-mediated generation of diacylglycerol initiated by the removal of cellular sphingomyelin and subsequently phosphorylates and stabilizes ABCA1
- the mitogen-activated protein kinase pathway is involved in the regulation of apoA-I gene expression by estrogen
- Data support the hypothesis of increased biliary catabolism of cholesterol in subjects with gallbladder disease characterized by lower Apo B and higher Apo A-I serum concentrations.
- Review. the formation, metabolism, and regulation of monomolecular, lipid-free/lipid-poor apoA-I in plasma.
- N-terminal deletion mutants of apoA-1, Delta(1-41) and Delta(1-59), show altered lipid-binding ability compared to plasma and wild-type apoA-I, and in double deletion mutants, Delta(1-41, 185-243) and Delta(1-59, 185-243), lipid binding is abolished.
- association of apolipoprotein A-I with lipids reduces its ability to interact with ATP-binding cassette transporter A1(ABCA1) and the lipid translocase activity of ABCA1 generates alpha-LpA-I-like particles
- FTD patients showed a significantly higher prevalence of low MW apo(a) isoforms than the cognitively healthy controls (P=0.011 and P=0.025, respectively). Our data suggest a role of apo(a) phenotypes of low MW in mediating susceptibility to FTD.
- Expression of Apo A1 is associated with colonic adenocarcinoma progression, and thus Apo A1 is a potential marker of the aggression.
- Apolipoprotein A-I activates cellular cAMP signaling through the ABCA1 transporter
- prebeta HDL that contains APOa1, but not APOa2, has two metabolic fates in vivo, rapid removal from plasma and catabolism by kidney or remodeling to medium-sized HDL
- ApoA-1 binds to lipid raft & nonraft domains of the macrophage plasma membrane. Cholesterol exported to apoA-1 from the major slow-efflux pool derives from nonraft regions but the interaction of apoA-1 with lipid rafts is needed to stimulate this efflux.
- expression in the heart; detection of apoA-I expression in the hearts of human apoA-I Tg mice indicates that the minimal regulatory elements necessary for cardiac expression of the gene are located near its coding sequence
- ApoA-I mutants that are poor cholesterol acceptors cross-link poorly to the ATP binding cassette transporter A1 (ATPCA1), affecting cholesterol efflux and inhibiting biogenesis of cholesterol high-density lipoproteins.
- alterations in transcriptional control of apo A-I in diabetes (review)
- ABCA1-independent but apoa1-dependent cholesterol removal pathway may help to prevent early atherosclerosis in Tangier disease.
- Apo A-I binding to lecithins and small unilamellar vesicles exhibits different helical structures.
- a specific structural element possessing a linear array of acidic residues spanning two apoA-I amphipathic alpha-helices is required to mediate cholesterol efflux and stabilize ABCA1
- alterations in apoA-I conformation can lead to aberrant trafficking and accumulation of apolipoprotein-phospholipid structures, and may underlie the reduced plasma HDL concentrations observed in individuals harboring deletion mutations within helix 6.
- analysis of a novel, ABCA-1-independent, positive feedback pathway for stimulation of potentially anti-atherogenic apoE secretion by alpha-helix-containing molecules including apoA-I and apoE
- Patient carrying the apolipoproteins A allele has an increased risk to develop coronary artery disease.
- apolipoprotein A-I has a role in protecting against endotoxin toxicity
- The orphan nuclear receptor liver receptor homolog-1 regulates APOAI transcription and affects cholesterol homeostasis.
- When LDL apoB-100 pool size is big, there is a higher apoA-I production rate. Slow chylomicron remnant clearance is associated with enhanced apoA-I fractional catabolic rate. Changes in intestinal lipoproteins may be important in determining HDL-C levels
- apoA-I mobilizes intracellular cholesterol for the ABCA1-mediated release from the compartment that is under the control of ACAT. The cholesterol mobilization process is presumably related to PKC activation by apoA-I.
- tested whether rare sequence variants of ABCA1, APOA1, and LCAT collectively contribute to variation in plasma levels of high density lipoprotein cholesterol; nonsynonymous sequence variants were significantly more common in individuals with low HDL-C
- Human apoA-I/C-III/A-IV transgenic rabbits may provide a reliable model for studies of the transcriptional regulation of the cluster, and for evaluating the effects of different agents on the expression of the three genes.
- APOA1 is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease.
- In chronic hepatitis B, plasma Apo A-I level is not a reliable indicator of fibrosis.
- Results describe a model for a putative hinge domain in the context of recent "belt" and "hairpin" models of apolipoprotein A-I structure in discoidal high-density lipoprotein particles.
- Heterozygosity for a novel apoA-I mutation underlies a detrimental lipoprotein profile that is associated with endothelial dysfunction, accelerated carotid arterial wall thickening, and severely enhanced CAD risk.
- pitavastatin efficiently increases apoA-I in the culture medium of HepG2 cells by promoting apoA-I production through inhibition of HMG-CoA reductase
- The first 44 residues of human apoA-I have a moderate lipid binding affinity and can form both disks in the presence of excess peptide and vesicles of varous sizes over a wide range of excess peptide:lipid ratios.
- inhibition of transforming growth factor-beta activation is required for stimulation of vascular smooth muscle cell proliferation and migration by apolipoprotein(a)
- ApoA-I structure was analyzed to detect the site bound by haptoglobin
- ApoA-I may have a regulatory role at sites of macrophage activation by T lymphocytes in inflamed RA synovial tissue. The biologic properties of apoA-I may include anti-inflammatory activities.
- results indicate that Tyr(192) is the predominant site of nitration and chlorination when MPO or ONOO(-) oxidizes lipid-free apoA-I but that only chlorination markedly reduces the cholesterol efflux activity of apoA-I
- These data provide a novel explanation for the apparent AD-protective effect of inheriting an epsilon2 APOE allele, and suggest that optimizing AT enrichment of CNS lipoproteins or devising APOAI mimetics may augment AT efficacy in treating AD.
- Among these genetic polymorphisms, TaqIB of CETP and MspI of apolipoprotein AI appeared to help significantly to identify diabetic individuals. In particular, the former may have an additional role in the primary prevention of coronary disease.
- the apoCIII enhancer regulates expression of apoAI, apo-CIII, and apoAIV but not apoAV in vivo; the entire cluster has roles in regulating lipid metabolism
- results suggest that the most efficient reaction between apoA-I and DMPC/DSPC occurs in particular bilayer conditions, probably when small fluid domains are nucleated within a continuous gel phase and interfacial packing defects are maximal
- Single Nucleotide Polymorphisms in apolipoprotein A-I is associated with variation in plasma triglyceride levels Coronary Arteriosclerosis
- analysis of the interfacial properties of ApoA-I at the triolein/water interface
- A molecular model was built for the lipid-free apoA-I monomer based on homology with proteins of similar sequence and known three-dimensional structures.
- An apoA-I(delta 89-99) deletion mutant generates a phenotype not encountered previously which affects maturation of high-density lipoprotein, inhibits activity of phospholipid transfer protein, and promotes accumulation of abnormal lipoprotein particles.
- In the absence of apoA-1 carboxyl-terminal residues 187-243, removal of residues 1-43 does not induce a major structural reorganization while retaining a protein fold that is consistent with a globular amphipathic alpha-helix bundle.
- study of apolipoprotein A-I secondary structural and functional properties
- biophysical analysis of human apolipoprotein A-I interaction with model membranes exhibiting lipid domains
- Changes in triglycerides were influenced by the apolipoprotein AI XmnI polymorphism (p = 0.04), suggesting a gene-diet interaction (p = 0.03)in hyperuricemia
- The protective behavior of apo A-I against vesicle aggregation and cholesterol nucleation in the presence of phospholipase C (PLC) depends on the relative concentrations of lipids (cholesterol and lecithin) and proteins (apo A-I and PLC).
- NDRG1 interacts with APO A-I and A-II and may have a role in the general mechanisms of HDL-mediated cholesterol transport
- A third molecule of apoA-I can form a hairpin in larger particles containing three molecules of apoA-I.
- analysis of how contact between the globular N-terminal fold and C-terminal domain of ApoA-I stabilizes its lipid-bound conformation
- Two MspI polymorphisms in the ApoA-I gene (G-75A and C83T) have been shown to be associated with plasma HDL-cholesterol levels.
- Apolipoprotein E secretion from macrophages in type 2 diabetes was reduced in patients with low plasma HDL and ApoA-I levels.
- oxidized apoAI can be used as an early marker for oxidative stress in humans
- genetic variation at the APOA1 gene promoter is associated with HDL subfraction redistribution resulting from exercise training.
- In this report, a relationship between ApoA-I, DM and ABCA1 has been emphasized.
- apoA-I (E136X) is a cause of HDL-C deficiency in the French Canadian population and is associated with premature CAD.
- ApoA-I can bind with relatively high affinity to curved phospholipid bilayer surfaces and to microemulsion particle surfaces.
- tyrosine modification of apoAI is not required for its myeloperoxidase-mediated inhibition of cholesterol acceptor activity
- the ABCA1 pathway is impaired by acrolein-induced apoA-I modification
- These results suggest that variants of APOA1 might influence the onset and the risk for AD.
- Lp(a) levels and Apo(a) isoforms may have roles in ischaemic stroke in the elderly
- 1, 25-(OH)2 D3 suppresses apo A1 gene expression at the transcriptional level, possibly by altering coactivators or corepressors. This effect requires the vitamin D receptor as well as a vitamin D response element in the apo AI promoter.
- The novel inhibitory function of apoA-I on DC differentiation and function may facilitate the development of new therapeutic interventions in inflammatory diseases.
- in the atherosclerosis-susceptible human apoB/A-II mouse model, expression of the human apoA-I(M) gene does not have protective advantage over that of the apoA-I gene.
- results support the presence of a discrete globular bundle conformation for lipid-free apo A-I
- Metabolic syndrome men exhibit hypercatabolism of the two major HDL lipoprotein particles, LpA-I and LpA-I:A-II.
- Review discusses clinical significance of different levels of Apo A1, its role in induction or protection from autoimmunity, and the presence of specific Apo A1 autoantibodies in different autoimmune diseases.
- Northern Indians harboring a -75 guanine to adenine base change might be at higher risk (compared to GG homozygotes) of developing severe forms of coronary artery disease with lower levels of HDL-cholesterol and apoA-I.
- findings show that serum opacity factor (SOF) interacts with HDL in human blood by binding to apoA-I and apoA-II and causing the release of HDL lipid cargo, which coalesces to form lipid droplets, resulting in opacification
- Results show that the products of the apoA-I/ABCA1 interaction include discoidal HDL particles containing different numbers of apoA-I molecules.
- Results suggest that ABCA1 transduces signals from apolipoprotein A-I (apoA-I) by complexing and activating Cdc42 and downstream kinases and, therefore, acts as a full apoA-I receptor.
- The crystal structure of lipid-free apoA-I at 2.4 A was described.
- Apo A-I/apolipoprotein B ratio may be an additional marker in the search for biological correlates of increased risk of violence.
- TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation.
- Exhaustive lysine acetoacetylation lowered apoAI's isoelectric point, profoundly disrupted its secondary and tertiary structure.
- oxidation by myeloperoxidase impairs the ability of apoA-I to promote cholesterol efflux by the ABCA1 pathway, suggesting that this oxidative process might contribute to foam cell formation and atherogenesis
- Active plasma phospholipid transfer protein is associated with apoA-I- but not apoE-containing lipoproteins.
- The apoB/A1 level, but not LDL-cholesterol, is inversely related to endothelium-dependent vasodilation in an elderly Swedish population.
- Strong negative correlation between adiponectin and apoA-I fractional catabolic rate, which can explain the positive link between HDL cholesterol and adiponectin.
- Membranotropic activity of apolipoprotein A-I is associated with the presence of amphipathic alpha-helix regions.
- In the looped belt model, with the exception of amino acids 134-145, apoA-I aligns with its counterpart high density lipoprotein in a helix 5-helix 5 registry, centered at position 139
- illustrate the impact of context-dependence on single nucleotide polymorphism selection for prediction of cardiovascular disea risk factor variability
- the variability in APOA1/C3/A4/A5 gene cluster may affect TG and HDL levels in women with type 2 diabetes
- ApoB/ApoA-1 ratio showed a significant relationship in children with a family history of very early myocardial infarction.
- an increase in apoB and decrease in apoAI secretion may in part contribute to the known atherogenicity of Ox-LDL through an elevated LDL/HDL ratio, a strong predictor of coronary risk in patients
- plasma homocysteine concentrations are negatively correlated with HDL-C and apoA-I in patients with coronary artery disease
- Thus, apo(a) may interact with intact fibrin through the Lys-independent and Lys-dependent mechanisms, while the COOH-Lys-dependent mechanism may prevail in the presence of fibrinolytic activity.
- NPC1 protein function is non-essential for the trafficking and removal of cellular cholesterol by ApoAI if the down-stream defects in ABCA1 and ABCG1 regulation in NPC disease cells are corrected using an LXR agonist
- Mechanisms behind the dominant negative phenotype associated with the expression of the L159R apoA-I protein in humans.
- Amyloid in the knee joint menisci is formed from Apo A-I that is produced by chondrocytes within the meniscal cartilage.
- ApoA-I was found significantly increased in the chlorpromazine-treated rats and decreased in the patients with treatment-resistant schizophrenia, which suggest that decreased levels of apoA-I might be associated with the pathology of schizophrenia.
- analysis of the structural heterogeneity in the N-terminal domain of apoA-I in solution
- glycation of apoA-I may adversely affect reverse cholesterol transport in subjects with diabetes.
- decreased cholesterol-total cholesterol ratio in the plasma of human apolipoprotein A-I transgenic Scavenger Receptors, Class B, Type I-/- mice is attributed to a reduction in LCAT reactivity with sphingomyelin-enriched HDL particles
- Finds decreasing risk of dementia with increasing ApoA-1 concentrations and joint effect of ApoA-1 and ApoE-1 gene on risk of dementia in Japanese American men.
- Efflux defects are frequent in low HDL syndromes, but the majority of HDL deficient subjects with cellular cholesterol efflux defects do not harbor ABCA1 mutations, suggesting that novel pathways contribute to this phenotype.
- Variation in the apolipoprotein (APO) APOA1/C3/A4/A5 gene cluster on decreases in plasma cholesterol levels over an 8-year follow-up study.
- 220-231 region of apoA-I is required for functional interactions between apoA-I & ABCA1 that are necessary for biogenesis of alphaHDL particles & amino-terminal domain that lacks 220-231 region can form pre-HDL particles in an ABCA1-independent process.
- apoA-I binds with DMPC LUVs to form small lipid-protein domains on the LUV; then the domains are released to form large disks, which can mature in the presence of additional apoA-I to form small disks
- Liver-directed adeno-associated virus vector (AAV2.8)-mediated gene transfer of wild type ApoA-I and ApoA-I Milano each significantly reduces atherosclerosis progression in transgenic hypercholesterinemic mice.
- Interaction of apoA-I with ABCA1 results in the simultaneous generation of pre-beta HDLs of discrete size and chemical composition.
- ApoA-I may play a beneficial role in nonischemic heart failure partly through an anti-inflammatory action.
- analysis of the structure of apolipoprotein A-I in high density lipoproteins [review]
- For the prediction of ONFH, it is useful to analyze ApoB C7623T and plasma apoB/ApoA1 ratio before the administration of steroids.
- Speciation of human plasma high-density lipoprotein (HDL): HDL stability and APOA1 partitioning.
- it appears that these incremental changes in the interaction between the N- and C-terminal ends of apoA-I stabilize its tertiary conformation in the lipid-free state as well as allowing it to unfold & sequester discrete amounts of phospholipid molecules.
- Bone morphogenetic protein-1 functions as a proprotein convertase to stimulate the conversion of newly secreted proapo A1 to its phospholipid binding form.
- Liver transplantation in a patient with hereditary variant apolipoprotein AI (apoAI) amyloidosis associated with a 50% decrease in production of variant apoAI.
- studies suggest that if the Milano variant of apoA-I offers greater atheroprotection than wild-type apoA-I, it is not attributable to greater cellular lipid mobilization
- Polymorphisms in ApoAI-CIII-AIV gene cluster are associated with risks of diabetes and coronary heart disease.
- ApolipoproteinA1-75 G/A (M1-) polymorphism is relatively common and may confer a potential risk for cardiovascular disease.
- Our results show that apoA-I cleavage by transthyretin may affect HDL biology and the development of atherosclerosis by reducing cholesterol efflux and increasing the apoA-I amyloidogenic potential.
- Changes of HDL-cholesterol and apo-AI/apo-E mRNA ratio could be a good indicator of liver damage and/or hepatic functional recovery post-orthotopic liver transplantation.
- Patients with familial combined hyperlipidemia have increased carotid intimamedia thickness, strongly related to the apoB/apoA-I ratio (apolipoprotein B/apolipoprotein A-I)
- the action of human PLTP in the presence of human apoA-I results in the formation of a dysfunctional HDL subfraction, which is less efficient in the uptake of cholesterol from cholesterol-laden macrophages.
- genetic variation of 3' flanking region of ApoA-I (PstI), 3' untranslated region of ApoC-III (SstI) and intron 2 of ApoA-IV (XbaI) in 193 angiographically diagnosed coronary heart disease Punjab patients
- Infection by Trypanosoma brucei brucei causes hemolysis that triggers activation of trypanosome lytic factor by formation of haptoglobin-related protein-hemoglobin complexes, enhancing binding, trypanolytic activity, and clearance of parasites
- APOA1 -75 G/A polymorphism is associated with gallstone disease and shows sex-specific differences
- in metabolic syndrome, apoA-I-poor, small, dense HDL3c exert defective protection of endothelial cells from oxLDL-induced apoptosis
- patients heterozygous for a cytosine insertion in exon 3 (c.49-50 ins C), result in a frame-shift and premature stop codon at position 26 of pro-Apo A-I (Q17PFsX10); novel mutation prevents the synthesis of Apo A-I
- Despite their very low HDL levels, apoA-I(M) carriers do not display typical features of impaired vascular function because of an improved activity of apoA-I(M) HDL in maintaining endothelial cell homeostasis
- R153P mutation of APOA1 is critical for a familial Hypoalphalipoproteinemia syndrome
- Human apoA-I transfer increases the number of circulating EPCs, enhances their incorporation into allografts, promotes endothelial regeneration, and attenuates neointima formation in a murine model of transplant arteriosclerosis
- Our results suggest an impact of the G-->A polymorphism at position -75 bp in the APOA1 gene on cognitive impairment, but not on the risk of Alzheimer's disease.
- higher Met(O) content in apoA-I from diabetic patients is consistent with increased levels of lipid peroxidation products in plasma in diabetes
- APOA1/C3/A5 haplotype represents an important locus for predicting risk of hypertriglyceridemia among Taiwanese
- apoA-I specifically mediates the continuous endocytic recycling of ABCA1
- A monomeric apoA-I molecule associated with three to four phospholipid molecules has similar properties to the lipid-free apoA-I molecule.
- Upregulation of ProApolipoprotein A1 is associated with brain metastases in lung cancer
- Lipoprotein Lp(a)levels and not apo(a) isoform size are significant independent predictors of coronary artery disease in young Asian Indians.
- The central domain of ApoAI is involved in cholesterol cell traffic and solubilization, and may require a Y-type charge distribution in polar face, as well as a correct helices-polar face orientation.
- A study in dizygotic twins reveals a locus on chromosome 15q that shows significant linkage to serum levels of apoA-I among Swedish females and adds to the understanding of variation in risk for atherosclerotic disease.
- ATP-binding cassette transporter (ABC) A1 is required for the lipidation of apolipoprotein A-I to generate high density lipoprotein (HDL).
- The diurnal variation of the cardiovascular risk markers apolipoprotein A1 and B and apo B/apo A1 ratio.
- Apolipoprotein B/AI ratio was the best diagnostic marker of metabolic syndrome.
- ApoE and ApoA1 gene variants may act synergistically to associate with risk and protection against coronary artery disease.
- Data show that cholesterol is a determinant of the structures of discoidal high density lipoproteins formed by the solubilization of phospholipid membranes by apolipoprotein A-I.
- An association of the apoAI -75 bp G/A and serum TG, LDL-C and apoA-I levels in Hei Yi Zhuang was observed in this study.
- The combination of mass spectrometry, molecular modeling, molecular dynamic analysis, and small-angle X-ray diffraction has provided additional structural information on apoA-I folding that complements previous approaches[review]
- These results suggest that karyopherin beta3 plays a crucial role in apo A-I secretion.
- evidence that CTSS sequence variations are associated with two human metabolic risk factors for cardiovascular diseases: plasma Apo-A1 and HDL-C concentrations.
- Niacin treatment was associated with significant increases in HDL apoA-I concentrations and production, as well as enhanced clearance of TRL apoB-100 and apoB-48.
- Interaction of apolipoprotein A-I (apoA-I) with ATP binding cassette transporter 1 imparts a unique conformation that partially determines the in vivo metabolic fate of apoA-I in transgenic mice.
- The degradation or metabolization of acute-phase proteins, apolipoprotein A-I, and alpha1-antitrypsin, is a common response to gastric inflammation irrespective of Hp infection.
- ApoA-I facilitates ABCA1 recycle/accumulation to cell surface by inhibiting its intracellular degradation and increases high density lipoprotein generation.
- The extraordinary ability of apolipoprotein A-I (apoA-I)-mimetic peptide 4F to bind pro-inflammatory oxidized lipids probably accounts for its remarkable anti-inflammatory properties.
- Pathways of cholesterol efflux using apoA-I as an acceptor make a predominant contribution to cholesterol export from macrophages in vivo.
- the apoCIII enhancer contributes to the maintenance of an active chromatin subdomain of the apoAI/CIII/AIV genes, but not apoAV
- Apolipoprotein(a) 14-15 pentanucleotide repeats predict elevated levels of lipoprotein(a) and a 3- and 2-fold increased risk of myocardial infarction and ischemic heart disease in the general population.
- Apolipoprotein A-I tryptophan substitution leads to resistance to myeloperoxidase-mediated loss of function.
- Levels of apo A-I and apo H are elevated in the vitreous fluid of diabetic patients and a higher expression of apo A-I and apo H mRNAs exists in the diabetic retina.
- oxidation of a single Met in apoA-I results in impaired LCAT activation
- structure of APOA1, in spheres vs. discoidal forms
- The present study aimed to elucidate the relationship of four single nucleotide polymorphisms (SNPs) in the Apo11q cluster, to plasma lipids and Coronary Artery Disease.
- human apo A-I transfer accelerates endothelial regeneration mediated via SR-BI expressing bone marrow-derived EPCs, thereby preventing allograft vasculopathy.
- Conformational flexibility of the N-terminal domain of APOA1 bound to spherical lipid particles is reported.
- ApoA1 overexpression is an early event in the retina of diabetic patients and can be involved in the physiopathology of diabetic retinopathy. In addition, RPE is the main source of ApoA1 within the retina.
- Endothelial lipase appears to promote apolipoprotein A-I-mediated cholesterol efflux through catalytic and noncatalytic-dependent mechanisms in maacrophages.
- Major effect of LY518674 on the production and clearance of apoA-I and high density lipoproteins despite no change in the plasma concentration.
- Phosphatidylinositol acts through MAPK pathways to increase plasma apo A-I levels by protecting it from reuptake and degradation.
- KV11 peptide (from human Apolipoprotein A) suppresses angiogenesis and tumor progression by targeting the c-Src/ERK signaling pathways in VEGF induced cells
- Apolipoprotein A1 gene A/A substitution at position -75 in promotor is associated with ANFH.
- Prognostic utility of apoB/AI, total cholesterol/HDL, non-HDL cholesterol, or hs-CRP as predictors of clinical risk in patients receiving statin therapy after acute coronary syndromes: results from PROVE IT-TIMI 22.
- The retroendocytosis pathway of ABCA1/apoA-I contributes to HDL formation when excess lipoprotein-derived cholesterol has accumulated in cells.
- Polymorphsms may increase risk of myocardial infarct.