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ABCA1ATP (Adenosine Triphosphate) Binding Cassette Transporter A1
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Recent studies showed that LXR[alpha] is considered as a critical regulator in cholesterol homeostasis in macrophages, which could regulate several genes involved in cholesterol transport, such as the ATP-binding cassette trans-porters (ABCs), ABCA1, ABCG1, apolipoprotein E (ApoE) and lipoprotein lipase (LPL) (Vinoda et al.
Figure 3 shows CYP7A1, ABCG8, NPC1L1, HMG-CoAR, SREBP-1c, ABCA1, and SR-BI mRNA levels in the liver determined by qRT-PCR.
Se ha reportado que las HDL remueven el colesterol libre de las balsas lipidicas, principalmente a traves de las proteinas transportadoras ABCA1 y ABCG1 (49), proceso regulado por un heterodimero conformado por los receptores X de higado y los receptores X retinoides.
Similar to the ABCA1 study, the decrease in HDL-C due to the LCAT SNP would also decrease LDL-C via the CETP pathway (56), further complicating the interpretation of these results regarding the role of low plasma HDL concentration and CVD risk.
A protein called ABCA1 is needed for macrophages to release cholesterol into the bloodstream.
This process is facilitated by passive diffusion of cholesterol toward HDL and actively by the interaction of lipoproteins poor in apolipoprotein A1 (ApoA1), preBetaHDL or ABCA1, which facilitates cholesterol removal (17).
COX-2 inhibitors reduce the expression of cholesterol 27-hydroxylase and ABCA1 in macrophages, as do traditional non-selective nonsteroidal anti-inflammatory drugs.
One potential mechanism implicating dysfunctional HDL in the pathogenesis of cardiovascular disease was suggested as malondialdehyde impairing the cholesterol transporter ABCA1 activity of apo A-I (5).
The gene ABCA1 is at the crossroads of the process that shuttles intracellular cholesterol outbound.
Efflux and atherosclerosis: the clinical and biochemical impact of variations in the ABCA1 gene.
Several of the loci that are significantly associated with changes in lipid concentrations are in or near genes in which mutations have been shown to cause mendelian syndromes affecting lipid concentrations [namely genes that encode the proteins apolipoprotein E, ABCA1, apolipoprotein A-V, Cholesterylester transfer protein (CETP), lipoprotein lipase and hepatic lipase].
Las HDL nacientes atraviesan el endotelio vascular de los tejidos perifericos, desde los cuales remueven el exceso de colesterol libre celular, en un procedimiento mediado por el transportador de membrana ABCA1 (Brewer et al.