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Validated All-in-One™ qPCR Primer for ABCA1(NM_005502.3) Search again
Product ID:
HQP004727
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ABC-1, ABC1, CERP, HDLCQTL13, HDLDT1, HPALP1, TGD
Gene Description:
ATP binding cassette subfamily A member 1
Target Gene Accession:
NM_005502.3(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.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The membrane-associated protein encoded by this gene is a member of the superfamily of ATP-binding cassette (ABC) transporters. ABC proteins transport various molecules across extra- and intracellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP, MRP, ALD, OABP, GCN20, White). This protein is a member of the ABC1 subfamily. Members of the ABC1 subfamily comprise the only major ABC subfamily found exclusively in multicellular eukaryotes. With cholesterol as its substrate, this protein functions as a cholesteral efflux pump in the cellular lipid removal pathway. Mutations in this gene have been associated with Tangier's disease and familial high-density lipoprotein deficiency. [provided by RefSeq].
Gene References into function
- function as a regulator rather than an active transporter
- in the presence of apoE, overexpression of ABCA1 modulates HDL as well as apoB-containing lipoprotein metabolism and reduces atherosclerosis in vivo
- contributes to the secretion of interleukin 1beta from macrophages
- a novel site in the human ABCA1 promoter involved in the regulation of ABCA1 gene expression.
- Role as a phosphatidylserine translocase
- Apo AI/ABCA1-dependent and HDL3-mediated lipid efflux
- ABCA1 regulatory variants influence coronary artery disease independent of effects on plasma lipid levels
- Helical apolipoproteins stabilize ATP-binding cassette transporter A1 by protecting it from thiol protease-mediated degradation.
- ABCA1 mutations can disrupt its direct interaction with apolipoprotein A-I.
- Increased ABCA1 activity protects against atherosclerosis. ABCA1(human transgenic)(+)ApoE(-/-) mice developed dramatically smaller, less-complex lesions as compared with their ApoE(-/-) counterparts.
- R1680W mutation associated with Tangier disease, phenotypes variable.
- REVIEW: ATP-binding cassette transporter A1 and cholesterol trafficking
- Dominant expression of ABCA1 on basolateral surface of Caco-2 cells stimulated by LXR/RXR ligands
- A novel serine (Ser-2054) on the ABCA1 protein crucial for PKA phosphorylation and for regulation of ABCA1 transporter activity.
- Recent data confirms that a single defective allele in ABCA1 may be assosiated with reduced HDL cholesterol and FHA.
- The association of FADD with ABCA1 provides an unexpected link between high density lipoprotein metabolism and an adaptor molecule mainly described in death receptor signal transduction.
- findings suggest an important role for hepatocyte basolateral membrane ABCA1 in the regulation of the levels of intracellular hepatic cholesterol, as well as plasma HDL
- ABCA1 plays an important role in artery wall cell-mediated modification/oxidation of LDL by modulating the release of reactive oxygen species from artery wall cells that are necessary for LDL oxidation.
- ABCA1 is regulated by PEST sequence-mediated calpain proteolysis that appears to be reversed by apolipoprotein-mediated phospholipid efflux
- Golgi is involved in ABCA1-mediated cholesterol efflux.
- examine the necessary structural features for a protein to promote lipid efflux by the ABCA1 transporter and find the amphipathic helix is a key structural motif for peptide-mediated lipid efflux from ABCA1, but there is no stereoselective requirement
- Results describe two new point mutations of the ABCA1 gene found in one patient with Tangier disease and the sibling of another Tangier disease patient.
- Genetic variability of ABCA1 influences development of Alzheimer's disease,possibly by interfering with CNS cholesterol homeostasis.
- Review. Transgenic mice with human ABCA1 genes are used to study its function in cholesterol transport, apo B lipoproteins, and atherosclerosis.
- The K allele was significantly more frequent in FH subjects without premature CHD than in FH subjects with premature CHD suggesting that the genetic variant R219K in ABCA1 could influence the development and progression of atherosclerosis in FH subjects.
- ABCA1 expression varies among tissues, and cholesterol conversion to hydroxycholesterol is an important mechanism for the maintenance of cholesterol homeostasis in fibroblasts
- While genotype-phenotype associations were not reproduced across populations and loci, V825I and M883I were clearly associated with coronary artery disease status in Malays with no effects on HDL-C or apoA1.
- hepatic overexpression of ABCA1 showed a selective increase in HDL cholesterol
- In this study we review how genetic variation at the ABCA1 locus affects its role in the maintenance of lipid homeostasis and the natural progression of atherosclerosis.
- regulation of ABCA1 mRNA levels exploits the use of alternative transcription start sites
- ABCA1 has a role in the low levels of HDL-cholesterol and overaccumulation of cellular lipids in Niemann-Pick Disease type C
- Phosphorylation of a pest sequence in ABCA1 promotes calpain degradation and is reversed by ApoA-I.
- results indicate that the K219 allele frequency of adenosine triphosphate binding cassette transporter 1 differs markedly between blacks and whites
- ABCA1-mediated vesicle release involves lipid raft plasma membrane domains
- ABCA1 is phosphorylated and stabilized in a pathway in which apoA-I activates PKC alpha by PC-PLC-mediated generation of diacylglycerol
- These studies indicate a direct role of retinoic acid receptor gamma/retinoid x receptor in induction of macrophage ABCA1.
- ABCA7 compensates the function of ABCA1 for release of cell cholesterol in a certain condition(s).
- ABCA1 gene sequence in a proband with very low HDL cholesterol and premature coronary heart disease family history revealed 2 mutations: G5947A (R1851Q) and single thymidine deletion in a polypyrimidine tract 33 to 46 bps upstream from start of exon 47
- Of special interest was our finding that the effects of compromised ABCA1 function on HDL were more pronounced in women than in men.
- 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
- results suggest that the interaction of apolipoproteins with ATP binding cassette transporter A1(ABCA1)-expressing cells activates JAK2 which enhances apolipoprotein interactions with ABCA1 and lipid removal from cells
- first demonstration of an association between ATP-binding cassette, sub-family A member 1 gene expression and fasting glucose concentration in vivo
- HDL(3) promotes ABCA1-mediated lipid efflux entirely through its lipid-poor fraction with pre-beta mobility
- the ABCA1 transporter has a role in cellular cAMP signaling with Apolipoprotein A-I
- an amphiphilic helical motif is the minimum structural requirement for a protein to stabilize ABCA1 against proteolytic degradation
- ApoA-1 removes excess cholesterol & phospholipids from macrophages by an active pathway involving ABCA1. The slow component of this efflux is the ABCA1-dependent process.
- ABCA1 converts pools of late endocytic lipids that retain NPC1 to pools that can associate with endocytosed apoA-I, and be released from the cell as nascent high density lipoprotein
- ABCA1 is essential for the biogenesis of high density-sized lipoprotein containing only apoE particles in vivo
- the K219 allele of the ABCA1 gene is an anti-atherogenic allele with increased cholesterol efflux activity
- Two polymorphisms were associated with plasma levels of ApoA1, 1 in the promoter (C-564T) and 1 in the coding (R1587K) regions, whereas only 1 polymorphism (R219K) was associated with the risk of myocardial infarction.
- A two step model of cholesterol efflux is suggested that can explain the functional interactions of ABCA1 with apoA-I and other cholesterol acceptors, based on formation of a tight complex between ABCA1 and its ligands.
- increased palmitate and stearate desaturation by stearoyl-CoA desaturase was associated with the destabilization of ABCA1 by saturated fatty acids palmitate and stearate
- ABCA1 G(-273)C polymorphism has a significant effect on the HDL-C level in the general Japanese population, but not on the incidence of myocardia infarction
- ABCA1 does not differentiate between cholesterol and beta-sitosterol and thus is not responsible for the selectivity of sterol absorption by the intestine
- Several single nucleotide polymorphisms spanning the ABCA1 gene modify Alzheimer disease risk.
- ATP-binding-cassette transporter A1 gene expression in macrophages is downregulated by statins
- ABCA1 is not requied for a positive feedback pathway for stimulation of potentially anti-atherogenic apoE secretion by alpha-helix-containing molecules including apoA-I and apoE
- The reciprocal inhibition of SR-BI and ABCA1 by BLT-4 and glyburide raises the possibility that these proteins may share similar or common steps in their mechanisms of lipid transport.
- probucol inactivates ABCA1 in the plasma membrane with respect to its function in mediating binding of and lipid release by apolipoprotein and with respect to proteolytic degradation by calpain
- Both mutations prevent normal trafficking of ABCA1, thereby explaining their inability to mediate apoA1-dependent lipid efflux
- conclude that intact ATP binding cassette transporter A1 (ABCA1) function is necessary for proper maturation of dense bodies in platelets
- the majority of ABCA1 exists as a tetramer that binds apoA; the homotetrameric ABCA1 complex constitutes the minimum functional unit required for the biogenesis of high density lipoprotein particles.
- 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
- Serum amyloid A promotes ABCA1-dependent and ABCA1-independent lipid efflux from cells.
- SREBP2 down-regulates ATP-binding cassette transporter A1 in vascular endothelial cells
- ABCA1 forms a complex with syntaxin 13 and flotillin-1, residing at the plasma membrane and in phagosomes
- ABCA1 is not required for apolipoprotein A-1-mediated endothelial cholesterol efflux from vascular endothelial cells.
- ABC transporter A1 has a role in regulating levels of HDL cholesterol
- We propose that the decreased level of ABCA1 protein is a key factor in the development of atherosclerotic lesions.
- The ABCA1 gene -565C>T polymorphism was associated with coronary atherosclerosis severity. This variant had an effect on ABCA1 promoter activity. Common ABCA1 variants contribute to interindividual variability in atherosclerosis susceptibility & severity
- apolipoprotein A-I chlorination markedly impairs ABCA1-dependent cholesterol transport
- The allelic frequencies of A and G of ABCA1 gene are 53.4% and 46.6% and the genetic polymorphisms of ABCA1 in Chinese Han ethnic population are significantly different from Caucasians residing in USA or Europe.
- type 2 diabetes is associated with ABCA1 gene polymorphisms in a Japanese population
- Catalytic subunits of SWI/SNF chromatin remodeling complex, BRG-1 and brahma, play significant roles in enhancing LXR/RXR-mediated transcription of ABCA1 via the promoter DR-4 element
- RhoA has a role in ABCA1-mediated cholesterol efflux
- Deficiency of macrophage ACAT1 accelerates atherosclerosis in apoE-/- mice but has no effect when hypercholesterolemia is corrected by apoE expression. ACAT1 deletion impairs ABCA1-mediated cholesterol efflux in macrophages regardless of apoE expression
- cholesterol efflux via the ABCA1/apoA-I pathway is enhanced by the GSL synthesis inhibitor PDMP
- analysis of headgroup-specific exposure of phospholipids in ABCA1-expressing cells
- The ABCA1-mediated reaction produced two distinct HDLs, large cholesterol-rich and small cholesterol-poor particles, and the former is more prominently dependent on the increase of ABCA1 expression
- The role of high levels of HDL cholesterol in protection against development of atherosclerosis is generally attributed to its role in reverse cholesterol transport, and the ATP binding cassette transporter A1 is a key element of this process.
- the internalization and trafficking of ABCA1 is functionally important in mediating cholesterol efflux from intracellular cholesterol pools
- Result exhibited an interaction of PON1 gene polymorphism A/B192 and ABCA1 genetic variation R219K on serum lipid level.
- dramatic decrease of ABCA1 protein, the key molecule of cholesterol efflux, in atheroma
- Glycolaldehyde and glyoxal strongly inhibited ABCA1-dependent transport of cholesterol from cells to apoA-I, while methylglyoxal had little effect.
- In this report, a relationship between ApoA-I, DM and ABCA1 has been emphasized.
- An amino acid substitution in ABCA1 is associated with low levels of HDL and diabetes mellitus, type 2.
- intracellular unsaturated acyl-CoA derivatives destabilize ABCA1 by activating a PLD2 signaling pathway
- the ABCA1 pathway is impaired by acrolein-induced apoA-I modification
- Based on the results of genome-wide screens, along with biological studies, we selected three genes as candidates for AD risk factors: ATP-binding cassette transporter A1 (ABCA1), cholesterol 25-hydroxylase (CH25H) and cholesterol 24-hydroxylase (CH24H).
- mABC1 protein plays a major role in cellular protection against oxidant stress.
- beta1-syntrophin acts through a class-I PDZ interaction with the C terminus of ABCA1 to regulate the cellular distribution and activity of the transporter
- ABCA1 plays a role in the pathogenesis of parenchymal and cerebrovascular amyloid pathology
- A review of functions and mutations of ABCA1 in Tangier disease.
- Glucocorticoid receptor ligands affected ABCA1 expression and cholesterol efflux from macrophages
- ABCA! polymorphisms and prognosis after myocardial infarction were analyzed in a young male cohort.
- Approximately 20% of French-Canadian patients with severe HDL deficiency are associated with a defective ABCA1.
- ABCA1-mediated efflux to serum responds to the pool of lipid-free/poor apolipoproteins
- Results show that the products of the apoA-I/ABCA1 interaction include discoidal HDL particles containing different numbers of apoA-I molecules.
- Impact of genetic variation on ABCA1 function.
- 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.
- ABCA1 upregulation in macrophages inhibits the progression of atherosclerotic lesions
- 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
- analysis of the biochemical basis of the mechanism for HDL formation mediated by ABCA1
- ABCA1 is a rate-limiting factor of HDL assembly and is regulated by transcriptional and post-transcriptional factors. Post-transcriptional regulation of ABCA1 involves modulation of its calpain-mediated degradation.
- data support the observation that ABCA1 polymorphisms influence cholesterol metabolism of the brain, but might not act as a major risk factor in Alzheimer's disease.
- Fluorescence resonance energy transfer and native plyacrylamide gel electrophoresis analytical techniques were employed to assess the quaternary structure of ABCA1
- This study suggest a gender-specific and APOE and UBQLN1 independent association between the ABCA1/R219K polymorphism and late-onset Alzheimer's disease.
- Suppression of both the ABCA1 and ABCG1 genes may indicate that unsaturated fatty acids suppress not only cholesterol efflux to apoA-I and thereby nascent HDL formation but also HDL-dependent cholesterol efflux from vascular cells.
- ABCA1 polymorphisms are associated with varying plasma levels of HDL-C in Pakistani individuals.
- ABCA1 is expressed in keratinocytes, where it is negatively regulated by a decrease in cellular cholesterol levels or altered permeability barrier requirements and regulated by activators of LXR, PPARs, and RXR or increases in cellular cholesterol levels
- REVIEW: the presence of ABCA1 and ABCG1 in the AP-3 pathway will have major impact for membrane phospholipid processing and HDL metabolism and their relation to disorders of lysosome-related organelles
- generation in vitro of 15 missense mutations that have been described in patients with Tangier disease and familial hypoalphalipoproteinemia. (ABCA1)
- The role of SREBP-2 in the regulation of ABCA1 transcription via generation of oxysterol ligands for liver X receptor is reported.
- ABCG1 and ABCG4 act in concert with ABCA1 to maximize the removal of excess cholesterol from cells and to generate cholesterol-rich lipoprotein particles
- hepatic overexpression of ABCA1 in low density lipoprotein receptor-KO mice leads to: 1) expansion of the pro-atherogenic apoB-lipoprotein cholesterol pool size via enhanced transfer of HDL-cholesterol to apoB-lipoproteins
- 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
- ABCA1 polymorphism is associated with the pathogenesis of coronary heart disease in Germany.
- Two genes of the cholesterol efflux system (ABCA1 and ABCG1) were down-regulated in HCAECs exposed to uraemic plasma.
- ABCA1 plays a significant role in the regulation of neuronal cholesterol efflux to apolipoprotein E discs.
- ROS and NF-kappaB, but not LXR, mediate the IL-1beta-induced downregulation of ABCA1 via a novel transcriptional mechanism, which might play an important role of proinflammation in the alteration of lipid metabolism.
- The results suggest the promoting effects of AngII on the forming of foam cells are in a dose-dependent manner via down-regulating the expression of ABCA1.
- Results show that ABCA1 mRNA expression increased in response to dexamethasone in primary rat hepatocytes however, the effect was absent or inhibitory in human HepG2 cells and THP-1 macrophages due to low glucocorticoid receptor levels.
- ABCA1 gene I823M polymorphism altered plasma HDL-C level and also modified the effect of low-HDL-C on the risk of CAD.
- This is the first study reporting the association of the ATP-binding cassette transporter A1 R230C variant with obesity and obesity-related comorbidities in the Mexican population.
- An obvious association between polymorphisms of ABCA1 gene and AD was found; the risk for AD was significantly decreased in K allele (RK+KK genotypes) or KK homozygote carriers compared with RR genotypes carriers.
- analysis of genetic variation in the ATP-binding cassette transporter A1, plasma lipids, and risk of coronary heart disease
- Results suggest that defective ABCA1 function in cholesterol-loaded macrophages is one potential contributor to the impaired reverse cholesterol transport process and the increased coronary heart disease risk in subjects with familial low HDL.
- Rare mutations in ABCA1 are associated with low HDL-C. However, at least 1 ABCA1 polymorphism (eg, E1172D) may contribute to the high HDL-C phenotype.
- Results suggest that R219K polymorphism in ABCA1 gene is not only associated with serum HDL-C and TG levels in healthy Chinese subjects in Chengdu area, but also with HDL-C level and TC/HDL-C ratio in subjects with endogenous HTG.
- an influence of common ABCA1 functional polymorphisms on age of symptom onset in coronary artery disease patients
- ABCA1 expression in human leukocytes and muscle is associated with physical activity and alcohol consumption, respectively
- Interaction of apoA-I with ABCA1 results in the simultaneous generation of pre-beta HDLs of discrete size and chemical composition.
- the relationship between ABCA1 genetic variants and Alzheimer's disease (AD), independently or in concert with the APOE epsilon4 allele
- Intronic polymorphism of ABCA1 gene is associated with sporadic Alzheimer's disease
- Taken together, the current study demonstrates that APN might protect against atherosclerosis by increasing HDL assembly through enhancing ABCA1 pathway and apoA-1 synthesis in the liver.
- Our study does not support a major role for the ABCA1 gene as a risk factor for ischaemic stroke
- Doxazosin inhibits AP2alpha activity independent of alpha(1)-adrenoceptor blockade and increases the ABCA1 expression and HDL biogenesis
- Our results provide a biochemical basis for the HDL biogenesis pathway that involves both ABCA1 and the "high-capacity binding site", supporting a two binding site model for ABCA1-mediated nascent HDL genesis.
- Results revealed that TNF-alpha could increase cholesterol content by down-regulating ABCA1 expression, IL-10 time-dependently decreased cholesterol accumulation by up-regulating ABCA1 expression.
- results indicate that ABCG5/G8, unlike ABCA1, together with bile acids should participate in sterol efflux on the apical surface of Caco-2 cells.
- R219K polymorphism of ABCA1 related with low HDL in overweight/obese Thai males.
- 3 of 6 nonsynonymous single nucleotide polymorphisms in ATP-binding cassette sub-family A (ABC1) member 1 (ABCA1) predict risk of ischemic heart disease in the general population.
- Experiments employing an ABCA1 promoter-luciferase reporter confirmed that ORP8 silencing enhances ABCA1 transcription and the silencing effect was partially attenuated by mutation of the DR4 element in the ABCA1 promoter.
- The interaction of ABCA1 with AOX1 modulates ABCA1-linked cellular functions such as lipid efflux and phagocytosis in hepatocytes (HC), and reduced expression of AOX1 in malignant transformed HC supports the differentiation dependent upregulation of AOX1
- plasma from men displayed an enhanced free cholesterol efflux capacity via the ABCA1 transporter pathway compared with that from women, which resulted from a 2.4-fold increase in the plasma level of prebeta particles
- These results suggest that polymorphisms of ABCA1 and ROS1 are determinants of blood pressure and the development of hypertension in Japanese individuals.
- Mutations were identified in 5 low-HDL subjects. 4 SNPs in ABCA1 gene promoter identified the C-14T SNP & the TCCT haplotype to be over-represented in low-HDL individuals. Sequence variation in ABCA1 contributes significantly to variation in HDL levels.
- apoA-I specifically mediates the continuous endocytic recycling of ABCA1
- ABC-A1 may be more than a determinant of HDL-cholesterol which may provide a link between components of the metabolic syndrome and atherosclerosis.
- Study of HDL particles formed when lipid-free apoA-I was incubated with fibroblasts in which expression of the ABCA1 was upregulated.
- ABCA1-dependent cholesterol efflux requires an amphipathic helical region of the N-terminal barrel of phospholipid transfer protein
- ABCA1 Q597R mutant trafficking to the plasma membrane was rapidly induced by thapsigargin or DTT, indicating that ER stress-induced QR trafficking.
- ATP-binding cassette transporter (ABC) A1 is required for the lipidation of apolipoprotein A-I to generate high density lipoprotein (HDL).
- Study results suggest that polymorphisms of ABCA1 C69T may be associated with plasma triacylglycerol and VLDL-cholesterol levels in coronary artery patients.
- Physical interaction of ABCA1 and SPTLC1 results in reduction of ABCA1 activity and that inhibition of this interaction produces enhanced cholesterol efflux.
- Lower plasma levels of HDL cholesterol due to heterozygosity for loss-of-function mutations in ABCA1 were not associated with an increased risk of IHD.
- 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.
- ApoA-I facilitates ABCA1 recycle/accumulation to cell surface by inhibiting its intracellular degradation and increases high density lipoprotein generation.
- No associations between fasting glucose, hemoglobin A(1c), plasma lipids, or oxLDL and the expression of ABCG1, ABCA1, or SR-BI were found in diabetic patients.
- Various studies have identified debatable and sometimes inconsistent results with respect to the risk on MI attributed by common genetic variation in ABCA1.
- ABCA1-mediated cholesterol efflux is independent of cholesterol synthesis
- Stimulation of hydrolysis of cholesteryl ester in macrophages induces the expression of ABCA1 gene primarily via the LXR-dependent pathway and can be useful for the prevention of atherosclerosis.
- Ability of the lipid transporter ABCA1 and apolipoprotein CIII to promote the de novo biogenesis of apoCIII-containing high density lipoproteins in vivo.
- Findings suggest that the endocytic ABCA1 has cholesterol efflux activity, and thus the cellular control of post-endocytic sorting, retention or recycling of ABCA1 in the endocytic vesicles is important for cholesterol metabolism in living cells.
- nuclear liver X receptor-beta interaction with ABCA1 modulates cholesterol efflux
- analysis of the specificity of ABCA1-dependent cholesterol efflux by peptides
- These findings establish a critical role for ABCA1 in reverse cholesterol and phospholipid transport in airway smooth muscle cells and suggest that dysregulation of cholesterol homeostasis in these cells may be important in the pathogenesis of diseases.
- the Y2206D mutation may be associated with not only a lower level of HDL-C, but also with dementia
- Single Nucleotide Polymorphism in ABCA1 is associated with susceptibility to radiation dermatitis in breast cancer.
- ABCA1 gene sequence together with a detailed sural nerve biopsy in a family from Afghanistan with a case of progressive syringomyelia-like phenotype and severe premature atherosclerosis.
- Results show no significant association between cardiovascular disease and ABCA1 gene A2589G and G3456C genotypes.
- Common genetic variations of ABCA1 had a moderate influence on HDL-C levels and/or coronary heart disease in patients with type 2 diabetes mellitus. These 2 effects were independent.
- study of the influence of ABCA1 and cholesteryl ester transfer protein genetic variants on lipoprotein subclasses demonstrates the importance of interpreting lipoprotein subclasses within the context of the biochemical processes
- although splice mutations in ABCA1 are uncommon, they are worthy of further consideration, particularly in cases where promoter and coding regions of candidate genes fail to identify the genetic basis of very low HDL-C
- The retroendocytosis pathway of ABCA1/apoA-I contributes to HDL formation when excess lipoprotein-derived cholesterol has accumulated in cells.