Official Symbol: APOA1provided by HGNC
Official Full Name: apolipoprotein A-Iprovided by HGNC
Primary Source: HGNC:600
See related: Ensembl:ENSG00000118137; HPRD:02517; MIM:107680
Gene type: protein coding
RefSeq status: REVIEWED
Organism: Homo sapiens
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo
Also known as: MGC117399; APOA1
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. Defects in this gene are associated with HDL deficiencies, including Tangier disease, and with systemic non-neuropathic amyloidosis. [provided by RefSeq]

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GeneRIFs: Gene References Into Function What's a GeneRIF?

	1.	Opacification of high density lipoproteins by recombinant serum opacity factor produces cholesteryl esters, neo high-density lipoprotein, and lipid-free apo A-I, all of which could enhance various reverse cholesterol transfer steps.
	2.	Results indicate that apo A-I(Milano) transfer is not superior compared to wild-type human apo A-I transfer.
	3.	CETP I405V polymorphism contributes to the unfavorable changes of apoA-I and HDL-C in a low polyunsaturated fat diet.
	4.	Data show that 12 SNPs from CETP, APOAI, ABCB1, CYP7A1, and HMGCR genes to be associated with baseline LDL-C and high-density lipoprotein cholesterol levels and increased risk of CAD.
	5.	apoAI/ prebHDL is a two-domain protein, including a N-terminal four helix bundle domain (residues 1-186) and a C-terminal flexible domain which display no well-defined structure (residues 187-243).
	6.	Nevirapine increases high-density lipoprotein cholesterol concentration by stimulation of apolipoprotein A-I production.
	7.	fatty acid-binding protein-5, squamous cell carcinoma antigens 2, alpha-enolase, annexin II, apolipoprotein A-I and albumin were detected at a high level in Atopic dermatitis skin lesions, but scarcely in the normal controls
	8.	apoA-I and apoB have roles in the pathogenesis of coronary disease
	9.	apoB and apoA-I may have a role in atherosclerotic progression
	10.	Low level of APO A-I is associated with a marked impairment of effective arterial volume, multiple organ dysfunction and a poor prognosis.
	11.	Retinol-binding protein is elevated in nondiabetic stage 5 chronic kidney disease and correlates weakly with HbA1c and ApoA1.
	12.	Model intimal arterial smooth muscle cells showed increased cholesteryl ester accumulation, absence of apolipoprotein A-I-mediated lipid efflux, markedly diminished ABCA1 expression, and poor apoA-I binding compared with medial-layer in atherosclerosis
	13.	high apoAI is associated with the manifestation of asthma and atopy.
	14.	Stimulation of cell surface F1-ATPase activity by apolipoprotein A-I inhibits endothelial cell apoptosis and promotes proliferation
	15.	at low pH. Trypanosome lytic factor, apoL-1, and apoA-1 exhibit specificity for anionic membranes, whereas Hpr permeabilizes both anionic and zwitterionic membranes.
	16.	most N-terminal region of apoA-I molecule, residues 1-43, contributes to the lipid interaction of apoA-I through the hydrophobic helical residues
	17.	Six patients with AApoAI amyloidosis due to APOA1 germline mutations that affect the larynx, small intestine, large intestine, heart, liver, kidney, uterus, ovary, or pelvic lymph nodes, are described.
	18.	in rheumatoid arthritis Apo A-I (apolipoprotein A-I) and Total Cholesterol levels are decreased in plasma and increased in Synovial fluid
	19.	ApoA-I-dependent cholesterol efflux mediated by ABCA1 requires formation of two intramolecular disulfide bonds
	20.	Plasma levels of apo(a) and Lp(a) display significant correlations with hepatic status
	21.	The frequency of the ApoAI and ApoB genetic polymorphisms has been reported for the first time in Tamilians (south Indians) and is distinct from other ethnic populations.
	22.	ABCA1-dependent lipid export, apolipoprotein A-I (apoA-I) binding, and signaling activities
	23.	Increased apo A-1 and apo B levels are associated in knee osteoarthritis, but the -460 T/C and +405 C/G VEGF polymorphisms are not associated with knee OA susceptibility.
	24.	APOA1 A-allele carriers displayed superior overall cognitive performance compared with non-carriers (P 0.008) and had a three-fold decrease in the relative risk of overall cognitive impairment in multiple sclerosis
	25.	These results show that apoA1 is consistently downregulated in the central nervous system as well as peripheral tissues of schizophrenia patients and may be linked to the underlying disease mechanism.
	26.	Very low density lipoprotein metabolism and plasma adiponectin as predictors of high-density lipoprotein apolipoprotein A-I kinetics in obese and nonobese men.
	27.	Polymorphsms may increase risk of myocardial infarct.
	28.	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
	29.	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.
	30.	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
	31.	The retroendocytosis pathway of ABCA1/apoA-I contributes to HDL formation when excess lipoprotein-derived cholesterol has accumulated in cells.
	32.	human apo A-I transfer accelerates endothelial regeneration mediated via SR-BI expressing bone marrow-derived EPCs, thereby preventing allograft vasculopathy.
	33.	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.
	34.	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.
	35.	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.
	36.	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.
	37.	Apolipoprotein A1 gene A/A substitution at position -75 in promotor is associated with ANFH.
	38.	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.
	39.	Major effect of LY518674 on the production and clearance of apoA-I and high density lipoproteins despite no change in the plasma concentration.
	40.	Endothelial lipase appears to promote apolipoprotein A-I-mediated cholesterol efflux through catalytic and noncatalytic-dependent mechanisms in maacrophages.
	41.	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.
	42.	Pathways of cholesterol efflux using apoA-I as an acceptor make a predominant contribution to cholesterol export from macrophages in vivo.
	43.	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.
	44.	KV11 peptide (from human Apolipoprotein A) suppresses angiogenesis and tumor progression by targeting the c-Src/ERK signaling pathways in VEGF induced cells
	45.	Clinical trial of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)
	46.	structure of APOA1, in spheres vs. discoidal forms
	47.	oxidation of a single Met in apoA-I results in impaired LCAT activation
	48.	Apolipoprotein A-I tryptophan substitution leads to resistance to myeloperoxidase-mediated loss of function.
	49.	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.
	50.	the apoCIII enhancer contributes to the maintenance of an active chromatin subdomain of the apoAI/CIII/AIV genes, but not apoAV
	51.	evidence that CTSS sequence variations are associated with two human metabolic risk factors for cardiovascular diseases: plasma Apo-A1 and HDL-C concentrations.
	52.	These results suggest that karyopherin beta3 plays a crucial role in apo A-I secretion.
	53.	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.
	54.	Lipoprotein Lp(a)levels and not apo(a) isoform size are significant independent predictors of coronary artery disease in young Asian Indians.
	55.	Phosphatidylinositol acts through MAPK pathways to increase plasma apo A-I levels by protecting it from reuptake and degradation.
	56.	Conformational flexibility of the N-terminal domain of APOA1 bound to spherical lipid particles is reported.
	57.	ApoA-I facilitates ABCA1 recycle/accumulation to cell surface by inhibiting its intracellular degradation and increases high density lipoprotein generation.
	58.	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]
	59.	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.
	60.	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.
	61.	A monomeric apoA-I molecule associated with three to four phospholipid molecules has similar properties to the lipid-free apoA-I molecule.
	62.	ApoE and ApoA1 gene variants may act synergistically to associate with risk and protection against coronary artery disease.
	63.	The diurnal variation of the cardiovascular risk markers apolipoprotein A1 and B and apo B/apo A1 ratio.
	64.	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.
	65.	ATP-binding cassette transporter (ABC) A1 is required for the lipidation of apolipoprotein A-I to generate high density lipoprotein (HDL).
	66.	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.
	67.	Apolipoprotein B/AI ratio was the best diagnostic marker of metabolic syndrome.
	68.	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.
	69.	apoA-I specifically mediates the continuous endocytic recycling of ABCA1
	70.	higher Met(O) content in apoA-I from diabetic patients is consistent with increased levels of lipid peroxidation products in plasma in diabetes
	71.	APOA1/C3/A5 haplotype represents an important locus for predicting risk of hypertriglyceridemia among Taiwanese
	72.	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
	73.	Upregulation of ProApolipoprotein A1 is associated with brain metastases in lung cancer
	74.	Patients with familial combined hyperlipidemia have increased carotid intimamedia thickness, strongly related to the apoB/apoA-I ratio (apolipoprotein B/apolipoprotein A-I)
	75.	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.
	76.	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.
	77.	R153P mutation of APOA1 is critical for a familial Hypoalphalipoproteinemia syndrome
	78.	in metabolic syndrome, apoA-I-poor, small, dense HDL3c exert defective protection of endothelial cells from oxLDL-induced apoptosis
	79.	Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)
	80.	Observational study of gene-disease association, gene-gene interaction, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)
	81.	Observational study and genome-wide association study of gene-disease association. (HuGE Navigator)
	82.	Observational study of gene-environment interaction and pharmacogenomic / toxicogenomic. (HuGE Navigator)
	83.	Observational study of genotype prevalence. (HuGE Navigator)
	84.	Observational study of gene-environment interaction. (HuGE Navigator)
	85.	Observational study of gene-disease association and gene-environment interaction. (HuGE Navigator)
	86.	Observational study of genotype prevalence and gene-disease association. (HuGE Navigator)
	87.	Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator)
	88.	Observational study of gene-disease association. (HuGE Navigator)
	89.	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
	90.	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.
	91.	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
	92.	APOA1 -75 G/A polymorphism is associated with gallstone disease and shows sex-specific differences
	93.	ApolipoproteinA1-75 G/A (M1-) polymorphism is relatively common and may confer a potential risk for cardiovascular disease.
	94.	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.
	95.	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.
	96.	glycation of apoA-I may adversely affect reverse cholesterol transport in subjects with diabetes.
	97.	For the prediction of ONFH, it is useful to analyze ApoB C7623T and plasma apoB/ApoA1 ratio before the administration of steroids.
	98.	Liver transplantation in a patient with hereditary variant apolipoprotein AI (apoAI) amyloidosis associated with a 50% decrease in production of variant apoAI.
	99.	Polymorphisms in ApoAI-CIII-AIV gene cluster are associated with risks of diabetes and coronary heart disease.
	100.	analysis of the structure of apolipoprotein A-I in high density lipoproteins [review]
	101.	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
	102.	Speciation of human plasma high-density lipoprotein (HDL): HDL stability and APOA1 partitioning.
	103.	Apo A-I mutations cannot be firmly establihed in samll number of patients with severe HDL deficiency.
	104.	biophysical analysis of human apolipoprotein A-I interaction with model membranes exhibiting lipid domains
	105.	Apolipoprotein A-II inhibits high density lipoprotein remodeling and lipid-poor formation of this protein
	106.	These results suggest that variants of APOA1 might influence the onset and the risk for AD.
	107.	analysis of the interfacial properties of ApoA-I at the triolein/water interface
	108.	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
	109.	mechanism for the induction of apoA-I might include PPAR-gamma for which oxidized fatty acid is a ligand.
	110.	APOAI had distinct inhibitory effects on the lipolysis of large and small emulsions: more effective inhibition for small emulsions.
	111.	Results show that during the early stages, oxidation of HDL gives rise to specifically oxidized forms of apolipoproteins A-I and A-II.
	112.	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.
	113.	Exhaustive lysine acetoacetylation lowered apoAI's isoelectric point, profoundly disrupted its secondary and tertiary structure.
	114.	Active plasma phospholipid transfer protein is associated with apoA-I- but not apoE-containing lipoproteins.
	115.	G/A polymorphism of the apo A-I promoter region affects not only baseline HDL-C concentrations but also its response to pravastatin treatment.
	116.	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.
	117.	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.
	118.	In chronic hepatitis B, plasma Apo A-I level is not a reliable indicator of fibrosis.
	119.	Changes in triglycerides were influenced by the apolipoprotein AI XmnI polymorphism (p = 0.04), suggesting a gene-diet interaction (p = 0.03)in hyperuricemia
	120.	Two MspI polymorphisms in the ApoA-I gene (G-75A and C83T) have been shown to be associated with plasma HDL-cholesterol levels.
	121.	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
	122.	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.
	123.	ApoA-I can bind with relatively high affinity to curved phospholipid bilayer surfaces and to microemulsion particle surfaces.
	124.	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
	125.	the mitogen-activated protein kinase pathway is involved in the regulation of apoA-I gene expression by estrogen
	126.	Metabolic syndrome men exhibit hypercatabolism of the two major HDL lipoprotein particles, LpA-I and LpA-I:A-II.
	127.	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.
	128.	Individuals with this protein are at a higher risk for schizophrenia.
	129.	The novel inhibitory function of apoA-I on DC differentiation and function may facilitate the development of new therapeutic interventions in inflammatory diseases.
	130.	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.
	131.	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.
	132.	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.
	133.	Patient carrying the apolipoproteins A allele has an increased risk to develop coronary artery disease.
	134.	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.
	135.	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
	136.	additive influence of mutant APOA1 and testosterone on plasma HDL-cholesterol
	137.	Apolipoprotein A-I activates cellular cAMP signaling through the ABCA1 transporter
	138.	The orphan nuclear receptor liver receptor homolog-1 regulates APOAI transcription and affects cholesterol homeostasis.
	139.	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.
	140.	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.
	141.	NDRG1 interacts with APO A-I and A-II and may have a role in the general mechanisms of HDL-mediated cholesterol transport
	142.	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
	143.	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
	144.	APOA1 has a varying conformational states as it adjusts from a discoidal to a spherical surface
	145.	pitavastatin efficiently increases apoA-I in the culture medium of HepG2 cells by promoting apoA-I production through inhibition of HMG-CoA reductase
	146.	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.
	147.	significance of G--->A polymorphism in gene promoter on serum high density lipoprotein cholesterol levels in Japanese hyperlipidemic subjects
	148.	Single Nucleotide Polymorphisms in apolipoprotein A-I is associated with variation in plasma triglyceride levels Coronary Arteriosclerosis
	149.	the ABCA1 pathway is impaired by acrolein-induced apoA-I modification
	150.	genetic variation at the APOA1 gene promoter is associated with HDL subfraction redistribution resulting from exercise training.
	151.	oxidized apoAI can be used as an early marker for oxidative stress in humans
	152.	Apolipoprotein E secretion from macrophages in type 2 diabetes was reduced in patients with low plasma HDL and ApoA-I levels.
	153.	Results show that the products of the apoA-I/ABCA1 interaction include discoidal HDL particles containing different numbers of apoA-I molecules.
	154.	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
	155.	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.
	156.	Strong negative correlation between adiponectin and apoA-I fractional catabolic rate, which can explain the positive link between HDL cholesterol and adiponectin.
	157.	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
	158.	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
	159.	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.
	160.	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.
	161.	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).
	162.	Hepatitis B virus (HBV) reduced steady-state levels of apolipoprotein AI mRNAs in two hepatoma cell lines
	163.	Expression of Apo A1 is associated with colonic adenocarcinoma progression, and thus Apo A1 is a potential marker of the aggression.
	164.	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.
	165.	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
	166.	ABCA1-independent but apoa1-dependent cholesterol removal pathway may help to prevent early atherosclerosis in Tangier disease.
	167.	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.
	168.	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
	169.	Effects of enrichment of fibroblasts with unesterified cholesterol on the efflux of cellular lipids to apolipoprotein A-I
	170.	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.
	171.	the variability in APOA1/C3/A4/A5 gene cluster may affect TG and HDL levels in women with type 2 diabetes
	172.	ApoB/ApoA-1 ratio showed a significant relationship in children with a family history of very early myocardial infarction.
	173.	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
	174.	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.
	175.	A third molecule of apoA-I can form a hairpin in larger particles containing three molecules of apoA-I.
	176.	study of apolipoprotein A-I secondary structural and functional properties
	177.	comparison of 5 natural point mutations illustrates that a specific sequence between amino acids 110 and 162 is required for LCAT activation
	178.	apolipoproteins appear to be a class of mediators that can participate in the regulation of the activity of neutrophils
	179.	tyrosine modification of apoAI is not required for its myeloperoxidase-mediated inhibition of cholesterol acceptor activity
	180.	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.
	181.	Degradation of phospholipid transfer protein (PLTP) and PLTP-generated protein by mast cell chymase impairs high affinity efflux of cholesterol from macrophage foam cells.
	182.	the structural organization of lipid-free apoA-I and the role of different domains in lipid binding, with comparisons to apoE
	183.	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
	184.	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.
	185.	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
	186.	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
	187.	apolipoprotein A-I has a role in protecting against endotoxin toxicity
	188.	ApoA-I structure was analyzed to detect the site bound by haptoglobin
	189.	inhibition of transforming growth factor-beta activation is required for stimulation of vascular smooth muscle cell proliferation and migration by apolipoprotein(a)
	190.	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
	191.	structure-function studies of variants
	192.	Apo A-I binding to lecithins and small unilamellar vesicles exhibits different helical structures.
	193.	APOA1 has a role in formation of nascent high density lipoprotein particles
	194.	Apo A-I/apolipoprotein B ratio may be an additional marker in the search for biological correlates of increased risk of violence.
	195.	The crystal structure of lipid-free apoA-I at 2.4 A was described.
	196.	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
	197.	The apoB/A1 level, but not LDL-cholesterol, is inversely related to endothelium-dependent vasodilation in an elderly Swedish population.
	198.	Membranotropic activity of apolipoprotein A-I is associated with the presence of amphipathic alpha-helix regions.
	199.	illustrate the impact of context-dependence on single nucleotide polymorphism selection for prediction of cardiovascular disea risk factor variability
	200.	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.
	201.	analysis of the structural heterogeneity in the N-terminal domain of apoA-I in solution
	202.	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.
	203.	Interaction of apoA-I with ABCA1 results in the simultaneous generation of pre-beta HDLs of discrete size and chemical composition.
	204.	Bone morphogenetic protein-1 functions as a proprotein convertase to stimulate the conversion of newly secreted proapo A1 to its phospholipid binding form.
	205.	Apo AI/ABCA1-dependent and HDL3-mediated lipid efflux
	206.	Infusion of APOA1 into fasting healthy male subjects activated FVII, increased TAT complex blood levels, and decreased HDL triglyceride blood levels.
	207.	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.
	208.	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.
	209.	APOA1 to APOB ratio is related to myocardial infarction and stroke
	210.	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
	211.	Mechanisms behind the dominant negative phenotype associated with the expression of the L159R apoA-I protein in humans.
	212.	Amyloid in the knee joint menisci is formed from Apo A-I that is produced by chondrocytes within the meniscal cartilage.
	213.	Variation in the apolipoprotein (APO) APOA1/C3/A4/A5 gene cluster on decreases in plasma cholesterol levels over an 8-year follow-up study.
	214.	apolipoprotein AI conformation required for systemic amyloidosis is described
	215.	alterations in transcriptional control of apo A-I in diabetes (review)
	216.	APOA1 is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease.
	217.	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.
	218.	apoA-I (E136X) is a cause of HDL-C deficiency in the French Canadian population and is associated with premature CAD.
	219.	The spatial organization of apolipoprotein A-I on the edge of discoidal high density lipoprotein particles: a mass specrometry study.
	220.	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.
	221.	In conclusion, 12% of Hypoalphalipoproteinemia subjects were found to carry mutations in apo A-I, LCAT, or GBA genes
	222.	APOA1 has a role in regulating ABCA1 expression in macrophages
	223.	Review. the formation, metabolism, and regulation of monomolecular, lipid-free/lipid-poor apoA-I in plasma.
	224.	analysis of how contact between the globular N-terminal fold and C-terminal domain of ApoA-I stabilizes its lipid-bound conformation
	225.	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).
	226.	Lp(a) levels and Apo(a) isoforms may have roles in ischaemic stroke in the elderly
	227.	results support the presence of a discrete globular bundle conformation for lipid-free apo A-I
	228.	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.
	229.	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
	230.	ApoA-I may play a beneficial role in nonischemic heart failure partly through an anti-inflammatory action.
	231.	Apolipoprotein A-I alpha -helices 7 and 8 modulate high density lipoprotein subclass distribution
	232.	Mutations may be associated with hypertension
	233.	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
	234.	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.
	235.	study of structural and functional homology between human apolipoprotein A-I and envelope proteins of human immunodeficiency virus type 1 in CD4 receptor binding
	236.	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.
	237.	Polymorphisms are not associated with severe aortic valve stenosis
	238.	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
	239.	In this report, a relationship between ApoA-I, DM and ABCA1 has been emphasized.
	240.	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.
	241.	plasma homocysteine concentrations are negatively correlated with HDL-C and apoA-I in patients with coronary artery disease

Submit: New GeneRIF Correction

[Top][Help]HIV-1 protein interactions

Protein	Interaction
1. Envelope surface glycoprotein gp120	Apolipoprotein A-1 competes with CD4 receptor binding to HIV-1 gp120 in human lymphocytes	PubMed
2. Nef	HIV-1 Nef impairs cholesterol efflux from macrophages and inhibits internalization of apolipoprotein A1 from the plasma membrane	PubMed

Go to the HIV-1, Human Protein Interaction Database

[Top][Help]Interactions

Description ..........
Product	Interactant	Other Gene	Complex	Source	Pubs

NP_000030.1	NP_000030.1	APOA1		HPRD	PubMed

NP_000030.1	NP_658985.1	APOA1BP		HPRD	PubMed

NP_000030.1	NP_663318.1	APOL1		HPRD	PubMed

NP_000030.1	NP_001494.2	GPLD1		HPRD	PubMed
Hepatitis C virus NS5A interacts with apolipoprotein apoA1.
NP_000030.1	AAQ86584.1	HCVgp1		BIND	PubMed
Hepatitis C virus NS5A interacts with apolipoprotein apoA1.
NP_000030.1	NP_751927.1	HCVgp1		BIND	PubMed

NP_000030.1	NP_006218.1	PLTP		HPRD	PubMed
Reconstituted Complex
BioGRID:106832	BioGRID:106537	ABCA1		BioGRID	PubMed
Co-crystal Structure
BioGRID:106832	BioGRID:106832	APOA1		BioGRID	PubMed
Affinity Capture-Western
BioGRID:106832	BioGRID:126103	APOA1BP		BioGRID	PubMed
Two-hybrid
BioGRID:106832	BioGRID:106838	APOC1		BioGRID	PubMed
Co-purification
BioGRID:106832	BioGRID:106816	APOF		BioGRID	PubMed
Co-purification
BioGRID:106832	BioGRID:114112	APOL1		BioGRID	PubMed
Affinity Capture-Western
BioGRID:106832	BioGRID:107397	CD40LG		BioGRID	PubMed
Affinity Capture-Western; Reconstituted Complex
BioGRID:106832	BioGRID:109083	GPLD1		BioGRID	PubMed
Affinity Capture-Western
BioGRID:106832	BioGRID:110121	LBP		BioGRID	PubMed
Reconstituted Complex
BioGRID:106832	BioGRID:110123	LCAT		BioGRID	PubMed
Two-hybrid
BioGRID:106832	BioGRID:120825	MAP7D1		BioGRID	PubMed
Two-hybrid
BioGRID:106832	BioGRID:111162	PDE1A		BioGRID	PubMed
Co-purification; Reconstituted Complex
BioGRID:106832	BioGRID:111374	PLTP		BioGRID	PubMed
Two-hybrid
BioGRID:106832	BioGRID:112197	SAA2		BioGRID	PubMed
Two-hybrid
BioGRID:106832	BioGRID:114322	TNFRSF10C		BioGRID	PubMed
Two-hybrid
BioGRID:106832	BioGRID:115144	TOMM20		BioGRID	PubMed

[Top][Help]General gene information

Markers

GDB:182584(e-PCR): Links: UniSTS:155398

GDB:374151(e-PCR): Links: UniSTS:156944

ECD03090(e-PCR): Links: UniSTS:284177

RH1581(e-PCR): Links: UniSTS:88085

GDB:434790(e-PCR): Links: UniSTS:157212

stSG601816(e-PCR): Links: UniSTS:444574

stSG601817(e-PCR): Links: UniSTS:444575

REN72933(e-PCR): Links: UniSTS:397733

REN72934(e-PCR): Links: UniSTS:397734

REN72935(e-PCR): Links: UniSTS:397735

REN72936(e-PCR): Links: UniSTS:397736

G44357(e-PCR): Links: UniSTS:95144

REN72937(e-PCR): Links: UniSTS:397737

REN72938(e-PCR): Links: UniSTS:397738

REN72939(e-PCR): Links: UniSTS:397739

REN72940(e-PCR): Links: UniSTS:397740

REN72941(e-PCR): Links: UniSTS:397741

REN72942(e-PCR): Links: UniSTS:397742

REN72943(e-PCR): Links: UniSTS:397743

REN72944(e-PCR): Links: UniSTS:397744

REN72945(e-PCR): Links: UniSTS:397745

REN72946(e-PCR): Links: UniSTS:397746

REN72947(e-PCR): Links: UniSTS:397747

REN72948(e-PCR): Links: UniSTS:397748

REN72949(e-PCR): Links: UniSTS:397749

REN72950(e-PCR): Links: UniSTS:397750

RH11465(e-PCR): Links: UniSTS:50642

ECD02000(e-PCR): Links: UniSTS:283101

ECD02278(e-PCR): Links: UniSTS:283378

Phenotypes

Amyloidosis, 3 or more types: MIM: 105200
Amyloidosis, 3 or more types: MIM: 107680
ApoA-I and apoC-III deficiency, combined: MIM: 107680
Corneal clouding, autosomal recessive: MIM: 107680
Hypertriglyceridemia, one form: MIM: 107680
Hypoalphalipoproteinemia: MIM: 604091
Common variants at 30 loci contribute to polygenic dyslipidemia: NHGRI GWA Catalog
Genome-wide scan identifies variation in MLXIPL associated with plasma triglycerides: NHGRI GWA Catalog
Newly identified loci that influence lipid concentrations and risk of coronary artery disease: NHGRI GWA Catalog
Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts: NHGRI GWA Catalog
A null mutation in human APOC3 confers a favorable plasma lipid profile and apparent cardioprotection: NHGRI GWA Catalog
Genome-wide association study identifies genes for biomarkers of cardiovascular disease: serum urate and dyslipidemia: NHGRI GWA Catalog
Six new loci associated with blood low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides in humans: NHGRI GWA Catalog

Genotypes

See APOA1 SNP Genotype Report

See APOA1 SNP Geneview Report

See APOA1 SNP Variation Viewer Report

Homology

Homologs of the APOA1 gene The APOA1 gene is conserved in chimpanzee, dog, cow, mouse, chicken, and zebrafish.

Map Viewer (Mouse)

Pathways

KEGG pathway: PPAR signaling pathway: 03320
Reactome Event:Hemostasis: REACT_604
Reactome Event:Metabolism of lipids and lipoproteins: REACT_602
Reactome Event:Transmembrane transport of small molecules: REACT_15518

Gene Ontology Provided by GOA

Function	Evidence
apolipoprotein A-I receptor binding	IPI	PubMed
beta-amyloid binding	IDA	PubMed
cholesterol binding	IDA	PubMed
cholesterol transporter activity	IEA
enzyme binding	IPI	PubMed
high-density lipoprotein binding	IEA
high-density lipoprotein receptor binding	IPI	PubMed
identical protein binding	IEA
lipid transporter activity	IEA
phosphatidylcholine-sterol O-acyltransferase activator activity	IDA	PubMed
phospholipid binding	IDA	PubMed

Process	Evidence
Cdc42 protein signal transduction	IDA	PubMed
G-protein coupled receptor protein signaling pathway	IDA	PubMed
adrenal gland development	IEA
blood vessel endothelial cell migration	IEA
cholesterol biosynthetic process	IEA
cholesterol efflux	IEA
cholesterol homeostasis	IMP	PubMed
cholesterol import	IMP	PubMed
endothelial cell proliferation	IEA
glucocorticoid metabolic process	IEA
high-density lipoprotein particle assembly	IDA	PubMed
high-density lipoprotein particle clearance	IC	PubMed
lipid metabolic process	IEA
lipid storage	IEA
lipid transport	IEA
lipoprotein biosynthetic process	IEA
negative regulation of cytokine secretion during immune response	IDA	PubMed
negative regulation of hydrolase activity	IEA
negative regulation of interleukin-1 beta secretion	IDA	PubMed
negative regulation of very-low-density lipoprotein particle remodeling	IDA	PubMed
phosphatidylcholine biosynthetic process	IDA	PubMed
phospholipid efflux	IDA	PubMed
phospholipid metabolic process	IEA
positive regulation of cholesterol esterification	IDA	PubMed
positive regulation of hydrolase activity	IDA	PubMed
positive regulation of transferase activity	IEA
protein stabilization	IDA	PubMed
regulation of intestinal cholesterol absorption	IEA
regulation of protein amino acid phosphorylation	IEA
reverse cholesterol transport	IMP	PubMed

Component	Evidence
cytoplasmic vesicle	IDA	PubMed
endocytic vesicle	IDA	PubMed
endoplasmic reticulum lumen	EXP	PubMed
extracellular region	EXP	PubMed
extracellular region	IEA
extracellular space	IEA
plasma membrane	EXP	PubMed
secretory granule	EXP	PubMed
spherical high-density lipoprotein particle	IDA	PubMed
very-low-density lipoprotein particle	IDA	PubMed

[Top][Help]General protein information

Preferred Names: apolipoprotein A-I

Names: apolipoprotein A-I; OTTHUMP00000069346; OTTHUMP00000069347; OTTHUMP00000069348

[Top][Help]NCBI Reference Sequences (RefSeq)

RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

Genomic

NG_012021.1 RefSeqGene

Range

5000..6869

Download

GenBank FASTA Sequence Viewer (Graphics)

mRNA and Protein(s)

NM_000039.1 → NP_000030.1 apolipoprotein A-I preproprotein

Source sequence(s)

X02162

Consensus CDS

CCDS8378.1

UniProtKB/Swiss-Prot

P02647

Conserved Domains (1) summary

pfam01442
Location:68 – 258
Blast Score: 467

Apolipoprotein; Apolipoprotein A1/A4/E domain

RefSeqs of Annotated Genomes: Build 37.1

The following sections contain reference sequences that belong to a specific genome build. Explain

Genome Reference Consortium Human Build 37 (GRCh37), Primary_Assembly

Genomic

NC_000011.9

Range

116706468..116708337, complement

Download

GenBank FASTA Sequence Viewer (Graphics)
NT_033899.8

Range

20268884..20270753, complement

Download

GenBank FASTA Sequence Viewer (Graphics)

Alternate assembly (Celera)

Genomic

AC_000054.1

Range

113864271..113866140, complement

Download

GenBank FASTA Sequence Viewer (Graphics)
NW_925173.1

Range

26733171..26735040, complement

Download

GenBank FASTA Sequence Viewer (Graphics)

Alternate assembly (HuRef)

Genomic

AC_000143.1

Range

112638728..112640597

Download

GenBank FASTA Sequence Viewer (Graphics)
NW_001838042.2

Range

4046411..4048280

Download

GenBank FASTA Sequence Viewer (Graphics)

[Top][Help]Related Sequences

Nucleotide		Protein
genomic	AF148963.1	AAD34604.1
genomic	AF485255.1	AAL92035.1
genomic	AP006216.1 (124799..126668)	None
genomic	AY422952.1	AAQ91811.1
genomic	AY555191.1	AAS68227.1
genomic	CH471065.1	EAW67274.1
		EAW67275.1
		EAW67276.1
		EAW67277.1
genomic	EF444948.1	ACA05932.1
		ACA05933.1
		ACA05934.1
		ACA05935.1
		ACA05936.1
genomic	J00098.1	AAB59514.1
genomic	J04066.1	AAA51746.1
genomic	X01038.1	CAA25519.1
genomic	X07496.1	CAA30377.1
mRNA	AK292231.1	BAF84920.1
mRNA	BC005380.1	AAH05380.1
mRNA	BC110286.1	AAI10287.1
mRNA	CR594974.1	None
mRNA	CR602459.1	None
mRNA	CR603689.1	None
mRNA	CR604796.1	None
mRNA	CR606088.1	None
mRNA	CR611719.1	None
mRNA	CR614893.1	None
mRNA	CR616175.1	None
mRNA	CR622099.1	None
mRNA	CR623518.1	None
mRNA	CR625742.1	None
mRNA	M11791.1	AAA35545.1
mRNA	M27875.1	AAA62829.1
mRNA	M29068.1	AAA51747.1
mRNA	X00566.1	CAA25232.1
mRNA	X02162.1	CAA26097.1
mRNA	A14829.1	CAA01198.1
mRNA	A15879.1	CAA01253.1
other-genetic	DQ893073.2	ABM83999.1
other-genetic	DQ896330.2	ABM87329.1

Protein Accession	Links
P02647.1	GenPept	UniProtKB/Swiss-Prot:P02647
Q6LEJ8	GenPept	UniProtKB/TrEMBL:Q6LEJ8
Q8TDB0	GenPept	UniProtKB/TrEMBL:Q8TDB0
Q9Y355	GenPept	UniProtKB/TrEMBL:Q9Y355