Редактирование: ABCG4 (раздел)

==Publications==

{{medline-entry
|title=Differential expression and function of [[ABCG1]] and [[ABCG4]] during development and aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19633360
|abstract=[[ABCG1]] and [[ABCG4]] are highly homologous members of the ATP binding cassette (ABC) transporter family that regulate cellular cholesterol homeostasis. In adult mice, [[ABCG1]] is known to be expressed in numerous cell types and tissues, whereas [[ABCG4]] expression is limited to the central nervous system (CNS). Here, we show significant differences in expression of these two transporters during development. Examination of beta-galactosidase-stained tissue sections from Abcg1(-/-)LacZ and Abcg4(-/-)LacZ knockin mice shows that [[ABCG4]] is highly but transiently expressed both in hematopoietic cells and in enterocytes during development. In contrast, [[ABCG1]] is expressed in macrophages and in endothelial cells of both embryonic and adult liver. We also show that [[ABCG1]] and [[ABCG4]] are both expressed as early as E12.5 in the embryonic eye and developing CNS. Loss of both [[ABCG1]] and [[ABCG4]] results in accumulation in the retina and/or brain of oxysterols, in altered expression of liver X receptor and sterol-regulatory element binding protein-2 target genes, and in a stress response gene. Finally, behavioral tests show that Abcg4(-/-) mice have a general deficit in associative fear memory. Together, these data indicate that loss of [[ABCG1]] and/or [[ABCG4]] from the CNS results in changes in metabolic pathways and in behavior.
|mesh-terms=* ATP Binding Cassette Transporter, Subfamily G
* ATP Binding Cassette Transporter, Subfamily G, Member 1
* ATP-Binding Cassette Transporters
* Aging
* Animals
* Behavior, Animal
* Brain
* Central Nervous System
* Conditioning, Classical
* Embryo, Mammalian
* Fear
* Gene Expression Regulation, Developmental
* Lipoproteins
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Microscopy, Electron, Transmission
* Retina
* beta-Galactosidase

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789777
}}
{{medline-entry
|title=Age-associated decrease of high-density lipoprotein-mediated reverse cholesterol transport activity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19405812
|abstract=High-density lipoproteins (HDL) are considered atheroprotective in contrast to low-density lipoproteins (LDL), which are atherogenic in their oxidized form. A growing body of evidence suggests that HDL exert part of their antiatherogenic effect by counteracting LDL oxidation as well as their proinflammatory effect. However, a number of studies, carried over the past 30 years, have shown that cholesterol efflux plays a major role in the atheroprotective effects of HDL and cholesterol homeostasis. These studies have further identified the scavenger receptor type B-I (SR-BI), the adenosine triphosphate (ATP)-binding cassette transporters ATP-binding cassette subfamily A1 ([[ABCA1]]), ATP-binding cassette subfamily G1 ([[ABCG1]]) and [[ABCG4]], the liver X receptor/retinoid X receptor (LXR/RXR) and peroxisome proliferator-activated receptorgamma(PPAR gamma) transcription factors, the HDL components apolipoprotein A-I (apoA-I), lecithin-cholesterol acyltransferase (LCAT), and phospholipids as additional mediators of cholesterol transport. Cholesterol efflux occurs via three independent pathways: (1) aqueous diffusion, (2) nonspecific efflux via SR-BI receptors, and (3) specific efflux via cholesterol-responsive members of the ABC superfamily. Whereas aqueous diffusion and scavenger receptor class B, type I (SR-BI)-mediated efflux transport free cholesterol to a wide variety of cholesterol acceptors (particles containing phospholipids, HDL, and lipidated apo-lipoproteins; LDL, etc), the [[ABCA1]] pathway mediates the transport of cholesterol in a unidirectional manner, mainly to lipid-poor apoA-I. In contrast, the [[ABCG1]] pathway is responsible for the transport of cholesterol to all the subfamily members of HDL. Although HDL-mediated cholesterol efflux is apoA-I-dependent, recent studies have suggested an involvement of the enzyme paraoxonase 1 ([[PON1]]). Cholesterol efflux is carried on by a number of factors such as genetic mutations, smoking, stress, and high-fat diets. It is attenuated with aging due to changes in the composition and structure of HDL, especially the phosphatidylcholine/sphingomyelin ratio, the fluidity of the phospholipidic layer, the concentration of apoA-I, and the activity of [[PON1]]. This review summarizes the findings that cholesterol homeostasis is disrupted with aging as a consequence of dysfunctional cholesterol efflux and the impairment of physiological functions.
|mesh-terms=* ATP-Binding Cassette Transporters
* Aging
* Animals
* Biological Transport
* Cardiovascular Diseases
* Cholesterol
* Humans
* Lipoproteins, HDL

|full-text-url=https://sci-hub.do/10.1089/rej.2009.0840
}}
{{medline-entry
|title=Distinct spatio-temporal expression of ABCA and ABCG transporters in the developing and adult mouse brain.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/16181433
|abstract=Using in situ hybridization for the mouse brain, we analyzed developmental changes in gene expression for the ATP-binding cassette (ABC) transporter subfamilies [[ABCA1]]-4 and 7, and [[ABCG1]], 2, 4, 5 and 8. In the embryonic brains, [[ABCA1]] and A7 were highly expressed in the ventricular (or germinal) zone, whereas [[ABCA2]], A3 and G4 were enriched in the mantle (or differentiating) zone. At the postnatal stages, [[ABCA1]] was detected in both the gray and white matter and in the choroid plexus. On the other hand, [[ABCA2]], A3 and A7 were distributed in the gray matter. In addition, marked up-regulation of [[ABCA2]] occurred in the white matter at 14 days-of-age when various myelin protein genes are known to be up-regulated. In marked contrast, [[ABCA4]] was selective to the choroid plexus throughout development. [[ABCG1]] was expressed in both the gray and white matters, whereas [[ABCG4]] was confined to the gray matter. [[ABCG2]] was diffusely and weakly detected throughout the brain at all stages examined. Immunohistochemistry of [[ABCG2]] showed its preferential expression on the luminal membrane of brain capillaries. Expression signals for [[ABCG5]] and G8 were barely detected at any stages. The distinct spatio-temporal expressions of individual ABCA and G transporters may reflect their distinct cellular expressions in the developing and adult brains, presumably, to regulate and maintain lipid homeostasis in the brain.
|mesh-terms=* ATP-Binding Cassette Transporters
* Aging
* Animals
* Animals, Newborn
* Brain
* Embryo, Mammalian
* Immunohistochemistry
* In Situ Hybridization
* Mice
* Mice, Inbred C57BL
* Tissue Distribution

|full-text-url=https://sci-hub.do/10.1111/j.1471-4159.2005.03369.x
}}