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TRAK2 is a novel regulator of LXR-mediated ABCA1 expression, cholesterol efflux, and HDL biogenesis. TRAK2 may therefore be an important target in the development of anti-atherosclerotic therapies.
Association of rs146292819 Polymorphism in ABCA1 Gene with the Risk of Coronary Artery Disease in Pakistani Population.
Our findings demonstrate that CYP2J2 improves cardiac function by increasing the concentration of circulating EETs, and boosting angiogenesis via the Jagged1/Notch1 signaling pathway in MI-induced heart failure.
first Tangier disease patient in Lebanon carrying a new pathogenic variant in ABCA1
Because GPS2 expression is down-regulated in some humans with obese and type 2 diabetes, the macrophage GPS-2/ABC-A1 pathway could be altered and contribute to atherogenesis
our findings indicated that acrolein-enhanced atherogenesis by increasing FMO3 which increased inflammatory responses and decreased ABCA1 in vitro can be alleviated by Hydroxytyrosol (HT), which may have a therapeutic potential for the treatment of atherosclerosis.
ABCA1 R230C T allele gene mutation is a protective in decreasing the risk of diabetes in Caucasians and ABCA1 C69T gene mutation markedly influences the level of lipid metabolism in diabetic patients.
ABCA1-mediated cholesterol efflux and apoB-lipoprotein secretion in the retinal pigment epithelium
This study identifies for the first time the implication of adipocyte ATP-binding cassette G1 (ABCG1) and A1 (ABCA1) cholesterol transporters in metabolic complications of obesity. Plasma membrane ABCA1 expressions in visceral adipose tissue were lower in the group of morbidly obese patients without metabolic syndrome, compared to lean patients.
deletions of the ABCA1 gene in patients with hypoalphalipoproteinemia
Metabolic syndrome-associated inflammation leads to the over-expression of miR-9-5p13 and that negatively influences ABCA1 expression, and HDL-driven cholesterol transport.
ABCA1 recruits V-ATPase to the plasma membrane where V-ATPase mediates apoA1 acidification and membrane remodeling that promote apoA1 unfolding and ABCA1-mediated HDL (high-density lipoprotein) biogenesis and lipid efflux.
ABCA1 is significantly overexpressed in patients at advanced stages of colorectal cancer, and its overexpression confers proliferative advantages together with caveolin-1 dependent-increased migratory and invasive capacities.
the level of plasma exosomal miR-30e and miR-92a was up-regulated in patients with atherosclerosis and negative correlate with the plasma cholesterol and ABCA1 level, which may provide a new biomarker for clinical diagnosis and treatment of coronary atherosclerosis.
Polymorphisms of rs4149339, rs4743763 and rs2472386 in ABCA1 and three lifestyle factors (physical activity, fried food intake, and dessert intake) were associated with CAD in people with dyslipidemia in southern China.
Eighty-three percent of patients with a damaging mutation in ABCA1 or APOA1 had evidence of atherosclerosis compared with 38.6% with low HDL-C without such a mutation. All these variant sare private or rare (minor allele frequency,0.005 in Exome Aggregation Consortium database), and only 1variant was shared by more than 1 patient.
Attenuated LRP1 function decreases ABCA1 and increases SR-B1 plasma membrane expression, which combined may explain reduced HDL-C levels in individuals with loss-of-function LRP1 variants.
A common variant rs2230806 of the ABCA1 gene affects the plasma triglyceride level in patients with severe dyslipidemia.
It focuses on current understanding of the structure-function relationships of human ABCA1 and the molecular mechanisms underlying HDL particle production.
AGE-albumin diminishes ABCA1 by accelerating its degradation through the proteasomal and lysosomal systems. This may increase lipid accumulation in macrophages by diminishing cholesterol efflux via RAGE signaling contributing to atherosclerosis in diabetes mellitus.
our results highlight the importance of the LXR/ABCA1 system in brain pericytes and suggest a new role for these cells in brain cholesterol homeostasis.
The expression and distribution of the bovine ABCA1 transporter using quantitative PCR and the sequencing of the entire ABCA1 coding region, including the proximal promoter region, are reported.
Aortic endothelial cells transcytose high-density lipoproteins by mechanisms that involve either SR-BI or ABCG1 but not ABCA1.
ABCA1 promoter variants affect transcription activity and plasma HDL level in pigs
ABCA1 was up-regulated in monocytes of hypercholesterolemic pigs via oxidized-LDL and prior to development coronary atherosclerosis.
Both region-specific and ubiquitous (ABCA1) phenotype changes were identified as early prelesional responses of the endothelium to hypercholesterolemia
CSL112 elevation of ABCA1-dependent efflux may target atherosclerotic plaque for cholesterol removal.
A high-fat diet induced fatty liver in mice (C57BL/6J) given Pegvisomant treatment. IGF1 treatment stimulated ABCA1 expression to improve cholesterol accumulation in these mice. These results show that the PI3K/Akt/FoxO1 pathway contributes to the regulation of ABCA1 expression in response to IGF1 stimulation that suppressed fatty liver in GH-deficient mice.
Hepatic overexpression of endothelial lipase lowers high-density lipoprotein but maintains reverse cholesterol transport via SR-BI/ABCA1-dependent pathways.
Findings find that in skeletal muscle the levels of ABCA1 contribute to regulate cellular cholesterol content, Akt phosphorylation, GLUT4 translocation and glucose uptake. These results suggest that the reduction in ABCA1 expression contributes to the anomalous cholesterol accumulation and altered glucose transport displayed by skeletal muscle in the insulin resistance condition.
The results of this study reveal E4/Abca1(+/-) TBI mice have a distinct response to injury, and unique gene networks are associated with APOE isoform, Abca1 insufficiency and injury.
Cell migration is negatively modulated by ABCA1
Low ABCA1 expression is associated with atherogenesis.
Adipocyte Abca1 is a key regulator of adipocyte lipogenesis and lipid accretion, likely because of increased adipose tissue membrane cholesterol, resulting in decreased activation of lipogenic transcription factors PPARgamma and SREBP1.
HSP70 promotes the progression of atherosclerosis in apoE-/- mice by suppressing the expression of ABCA1 and ABCG1 through the JNK/Elk-1 pathway.
It was concluded that quercetin inhibits oxLDLinduced lipid droplets in RAW264.7 cells by upregulation of ABCAl, ABCG1, LXRalpha and downregulation of PCSK9, p53, p21 and p16.
these results suggest that apigenin may attenuate atherogenesis through up-regulating ABCA1-mediated cholesterol efflux and inhibiting inflammation.
TMP upregulated the protein stability of ABCA1 without affecting ABCG1. Accordingly, TMP regulated the expression of SR-A, CD36, ABCA1 and ABCG1 in aortas of ApoE-/- mice, which resembled the findings observed in macrophages.
HDL3, by interacting with ABCA1, modulates the miR143/145-myocardin axis and prevents the cholesterol-induced gene expression modification in smooth muscle cells regardless of its cholesterol unloading capacity.
(1) ABCA1 maintains optimal hepatocyte PM FC, through intracellular FC trafficking, for efficient insulin signaling; and (2) hepatocyte ABCA1 deletion produces a form of selective insulin resistance so that lipogenesis is suppressed but glucose metabolism remains normal
demonstrates behavior deficits caused by Abca1 deletion in APP/PS1DeltaE9 mouse model at an early stage of amyloid pathology. The basal deficits of Abca1ko, manifested by diminished cognitive performance, prevent them from coping with additional stressors, which is in part due to the impairment of neurite morphology in the hippocampus.
Rutaecarpine was identified to be a candidate that protected ApoE(-/-) mice from developing atherosclerosis through preferentially promoting activities of ABCA1 and SR-BI within RCT.
Abca1 has a protective role in atherosclerosis, it exerts detrimental effects on cardiac function after myocardial infarction
Caveolin-1 enhances internalization and degradation of ABCA1 by its association with ABCA1
ABCA1-derived nascent high-density lipoprotein-apolipoprotein AI and lipids metabolically segregate.
an important role for hepatic ABCA1 in regulating secretory trafficking and modulating VLDL expansion during the TG accretion phase of hepatic lipoprotein particle assembly
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.
ATP-binding cassette sub-family A member 1
, ATP-binding cassette transporter A1
, cholesterol efflux regulatory protein
, ATP-binding cassette, sub-family A (ABC1), member 1
, ATP-binding cassette, sub-family A member 1
, ATP-binding cassette transporter 1
, Cholesterol efflux regulatory protein
, ATP-binding cassette transporter
, ATP-binding cassette, sub-family A member 1-like
, ATP-binding cassette sub-family A member 1-like
, ATP-binding cassette 1
, ATP-binding cassette, sub-family A (ABC1), member 1B