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The protein encoded by ABCG1 is a member of the superfamily of ATP-binding cassette (ABC) transporters. Additionally we are shipping ABCG1 Antibodies (100) and ABCG1 Kits (33) and many more products for this protein.
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Aortic endothelial cells transcytose high-density lipoproteins by mechanisms that involve either SR-BI (show SCARB1 Proteins) or ABCG1 but not ABCA1 (show ABCA1 Proteins).
ABCG1 regulates pulmonary surfactant metabolism
Hepatic free cholesterol content was significantly increased in NASH (show SAMSN1 Proteins) as compared to non-NASH (show SAMSN1 Proteins) subjects, while ABCA1 (show ABCA1 Proteins) and ABCG1 protein levels significantly decreased with NASH (show SAMSN1 Proteins) and fibrosis progression. The relative expression of miR (show MLXIP Proteins)-33a and miR (show MLXIP Proteins)-144 correlated inversely with ABCA1 (show ABCA1 Proteins) but not with ABCG1 protein levels. miR (show MLXIP Proteins)-33a/144 and their target gene ABCA1 (show ABCA1 Proteins) may contribute to the pathogenesis of NASH (show SAMSN1 Proteins) in morbidly obese subjects.
Understanding the relationship between cholesterol and inflammation in the lung, and the role that ABC (show ABCB6 Proteins) transporters play in this may illuminate new pathways to target for the treatment of inflammatory lung diseases
Findings suggest that the ABCG1-mediated efflux of cholesterol, but not of 7-ketocholesterol, shows specificity for structural domains of apoA-I (show APOA1 Proteins) bound to reconstituted HDL (show HSD11B1 Proteins). Although the mid region alone of apoA-I (show APOA1 Proteins) associated to rHDL can promote ABCG1-mediated cholesterol efflux, deletion of carboxyl-terminal region 185-243 from full-length apoA-I (show APOA1 Proteins) diminishes ABCG1-mediated cholesterol efflux.
ABCG1 regulates T cell differentiation into Tregs, highlighting a pathway by which cholesterol accumulation can influence T cell homeostasis in atherosclerosis
Data show that ELOVL7, SOCS3 (show SOCS3 Proteins), ACSL4 (show ACSL4 Proteins) and CLU (show CLU Proteins) were upregulated while PRKAR1A (show PRKAR1A Proteins) and ABCG1 were downregulated in the phlegm-dampness group.
ABCG1 and ABCG4 (show ABCG4 Proteins) alter the distribution of gamma-secretase on the plasma membrane, leading to the decreased gamma-secretase activity and suppressed Abeta (show APP Proteins) secretion
Both the full-length and the short isoforms of ABCG1 can dimerize with ABCG4 (show ABCG4 Proteins), whereas the ABCG2 multidrug transporter is unable to form a heterodimer with ABCG4 (show ABCG4 Proteins).
DNA methylation (show HELLS Proteins) at the ABCG1 locus cg06500161 in blood DNA was associated with an increased risk for future type2 diabetes.
we have newly identified a haplotype-tagging SNP, rs225396, in ABCG1 to be associated with PCV and nAMD in Chinese and Japanese cohorts. This provides new evidence to support ABCG1 as a susceptibility gene for PCV and nAMD.
Our data indicate that a combination of vildagliptin and pravastatin significantly induces the expression of LXR (show NR1H3 Proteins)-ABCA1 (show ABCA1 Proteins)/ABCG1 cascade and improves cholesterol efflux (P > 0.05) in adipocytes. Our data may explain, at least in part, the improvement in HDL (show HSD11B1 Proteins)-C levels observed in patients receiving both medications
ABCG1 may play a protective role in early-stage atherosclerosis by reducing endothelial activation induced by oscillatory shear stress via suppressing the inflammatory response.
Endothelial cholesterol efflux pathways mediated by ABCA1 and ABCG1 are nonredundant and atheroprotective, reflecting preservation of endothelial NO synthase activity and suppression of endothelial inflammation, especially in regions of disturbed arterial blood flow.
ABCG1, irrespective of either a leucine or proline at position 550, is an intracellular protein (show CKAP2 Proteins) that localizes to vesicles of the endosomal pathway where it functions to mobilize sterols away from the endoplasmic reticulum and out of the cell.
our study suggests that MEK1/2 inhibitors activate macrophage ABCG1 expression/RCT, and inhibit foam cell formation and lesion development by multiple mechanisms, supporting the concept that ERK1/2 inhibition is anti-atherogenic
miR-33 augments macrophage lipid rafts and enhances proinflammatory cytokine induction and NF-kappaB activation by LPS. This occurs through an ABCA1- and ABCG1-dependent mechanism and is reversible by interventions upon raft cholesterol and by ABC transporter-inducing liver X receptor agonists.
ABCG1 expression was down-regulated by TLR4 (show TLR4 Proteins), which induces inflammation and lipid accumulation in vascular smooth muscle cells via PPARgamma (show PPARG Proteins)/LXRalpha (show NR1H3 Proteins) signaling.
Visfatin (show NAMPT Proteins) upregulated CD36 (show CD36 Proteins) and SRA (show MSR1 Proteins) expression and downregulated ABCA1 (show ABCA1 Proteins) and ABCG1 expression, subsequently increased ox-LDL uptake and decreased cholesterol efflux, and finally promoted foam cell formation via the PI3K- and ERK (show EPHB2 Proteins)-dependent pathways.
The 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 intra-cellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP, MRP, ALD, OABP, GCN20, White). This protein is a member of the White subfamily. It is involved in macrophage cholesterol and phospholipids transport, and may regulate cellular lipid homeostasis in other cell types. Six alternative splice variants have been identified.
ATP-binding cassette sub-family G member 1
, ATP-binding cassette, sub-family G (WHITE), member 1
, ATP-binding cassette sub-family G member 1-like
, ABC transporter 8
, ATP-binding cassette transporter 8
, ATP-binding cassette transporter member 1 of subfamily G
, homolog of Drosophila white
, white protein homolog (ATP-binding cassette transporter 8)
, ATP-binding cassette 8
, ATP-binding cassette, subfamily G, member 1
, white protein homolog