Disease relevance of Abcg1

• In contrast to their wild-type littermates, male Abcg1-/- mice exhibited no high-fat diet-induced impairment of glucose tolerance and fatty liver [1].
• However, the disruption of a single gene, which encodes the gamma chain of the Fc receptor, was found to achieve this uncoupling in a spontaneous model of lupus nephritis, the New Zealand Black/New Zealand White (NZB/NZW) mouse [2].
• Preautoimmune New Zealand Black/White (NZB/NZW) mice immunized with Escherichia coli (EC) double standard (ds) DNA produce antibodies that bind mammalian dsDNA and display specificities similar to spontaneous lupus anti-DNA [3].
• Dehydroisoandrosterone, administered orally to New Zealand Black/New Zealand White F1 hybrid mice, prevented the formation of antibodies to double-stranded DNA and prolonged survival in this murine model of lupus erythematosus [4].
• Prevention of glomerulonephritis and prolonged survival in New Zealand Black/New Zealand White F1 hybrid mice fed an essential fatty acid-deficient diet [5].

Psychiatry related information on Abcg1

• LR White embedding allows a multi-method approach to the analysis of brain tissue from patients with Alzheimer's disease [6].

High impact information on Abcg1

• Interestingly, this element can be spliced to C beta 2 in the New Zealand White mouse, in which the C beta 1 gene is deleted [7].
• The recent molecular analysis of several White Spotting and Steel alleles has provided insights into the mechanism of c-kit ligand-mediated processes, including cell proliferation, cell migration and cell survival [8].
• The c-kit receptor and its recently identified ligand are allelic with the murine White Spotting and Steel loci, respectively [8].
• Erythema migrans (EM), persistent skin infection, and visceral dissemination can be induced reproducibly in the adult male New Zealand White rabbit by intradermal injection of as few as 10(3) Borrelia burgdorferi [9].
• F1 hybrid offspring of New Zealand Black mothers and New Zealand White fathers [(NZB X NZW)F1] female mice develop antibodies to single-stranded (ss) and native DNA, immune complex glomerulonephritis, massive proteinuria, and premature death with renal failure [10].

Chemical compound and disease context of Abcg1

• We recently reported that Tva, the host cell receptor for subgroup A avian leukosis and sarcoma viruses, binds specifically to the subgroup A envelope glycoprotein (Env-A) (J.M. Gilbert, P. Bates, H. E. Varmus, and J. M. White, J. Virol. 68:5623-5628, 1994) [11].
• The susceptibility of Swiss White mice to colonization with Streptococcus (Enterococcus) faecalis was greatly increased when the animals were given 5 mg of streptomycin sulfate per ml in their drinking water [12].
• 2. At the onset of nephritis, at about 5 months of age, New Zealand Black/White F1 mice were divided in two groups that received either methylprednisolone or saline injections for 5 months [13].
• Intrauterine growth retardation, without an increase in gross abnormalities, was also observed in the offspring of pregnant New Zealand White rabbits dosed during the preimplantation stages of pregnancy with an "environmental cocktail" composed of ethanol, nicotine, caffeine, sodium salicylate, and dichloro-diphenyl-trichloro-ethane (DDT) [14].
• The anti-E. coli O157:H7 IgY was harvested from eggs laid by hens (23 weeks of age, Single Comb White Leghorn) immunized with formalin-killed E. coli O157:H7 [15].

Biological context of Abcg1

• The demonstration that Abcg1(-/-) macrophages undergo accelerated apoptosis provides a mechanism to explain the decrease in the atherosclerotic lesions [16].
• The murine Abcg1 gene is reported to consist of 15 exons that encode a single mRNA (herein referred to as Abcg1-a) and protein [17].
• In NZO mice, an Abcg1 variant was identified in a suggestive adiposity quantitative trait locus and was associated with higher expression of the gene in white adipose tissue [1].
• Cyp26A1 expression is inducible by RA, and the locus has previously been shown to contain a RARE (RA response element), R1, within the minimal promoter [Loudig, Babichuk, White, Abu-Abed, Mueller and Petkovich (2000) Mol. Endocrinol. 14, 1483-1497] [18].
• Eight of approximately 100 cell lines derived at the Scott and White Clinic from human solid tumors were found to have the same phenotypes when analyzed for 15 polymorphic enzymes at the Sloan-Kettering Institute for Cancer Research. These data were confirmed at the M [19].

Anatomical context of Abcg1

• CONCLUSIONS: These studies reveal an inverse relationship between Abcg1 expression and apoE accumulation and secretion in macrophages [20].
• Plasma apoE levels were markedly increased in recipients of Abcg1(-/-) bone marrow [20].
• OBJECTIVE: The lungs of Abcg1(-/-) mice accumulate macrophage foam cells that contain high levels of unesterified and esterified cholesterol, consistent with a role for ABCG1 in facilitating the efflux of cholesterol from macrophages to high-density lipoprotein (HDL) and other exogenous sterol acceptors [16].
• The reduction of adipose tissue mass in Abcg1-/- mice was associated with markedly decreased size of the adipocytes [1].
• Targeted disruption of Abcg1 in mice has no effect on plasma lipids but results in massive accumulation of both neutral lipids and phospholipids in hepatocytes and in macrophages within multiple tissues following administration of a high-fat and -cholesterol diet [21].

Associations of Abcg1 with chemical compounds

• Insertion of modified transposable elements of the P-family upstream of CG17646, the Drosophila ortholog of Abcg1, generated lines of flies with increased triglyceride stores [1].
• To examine the in vivo effects of a kinase-deficient mutant human insulin receptor, we used the muscle creatine kinase promoter to express a putative dominant-negative receptor: Ala1134-->Thr (Moller, D. E., Yokota, A., White, M. F., Pazianos, A. G., and Flier, J. S. (1990) J. Biol. Chem. 265, 14979-14985) in transgenic mice [22].
• Autoimmune female New Zealand Black/New Zealand White mice were treated with frentizole, an experimental immunosuppressive drug [23].
• Tumor necrosis factor and IL-1 in New Zealand Black/White mice. Enhanced gene expression and acceleration of renal injury [24].
• New Zealand White rabbits (n = 33) were given TGF-beta(2) (1.7 or 5.0 microg), talc (400 mg/kg), doxycycline (10 mg/kg), or buffer intrapleurally [25].

Other interactions of Abcg1

• Abca1 knockdown prevented the increase in apoE secretion but had minimal effects on apoE accumulation in cell lysates of Abcg1(-/-) macrophages [20].
• METHODS AND RESULTS: Bone marrow from Abcg1(-/-) mice was transplanted into irradiated Ldlr(-/-) recipients, and atherosclerosis was evaluated by aortic root assay after 7 or 11 weeks of feeding on a Western diet [20].
• METHODS AND RESULTS: Bone marrow from wild-type or Abcg1(-/-) mice was transplanted into Ldlr(-/-) or ApoE(-/-) mice [16].
• Sle1 on chromosome 1 and Sle3/5 on chromosome 7 are two of the most critical lupus susceptibility loci of the New Zealand Black/White-derived NZM2410 mouse strain [26].
• These SDKs were previously shown to phosphorylate endogenous 14-3-3 proteins (Megidish, T., White, T., Takio, K., Titani, K., Igarashi, Y., and Hakomori, S. (1995) Biochem. Biophys. Res. Commun. 216, 739-747) [27].

Analytical, diagnostic and therapeutic context of Abcg1

• Surprisingly, transplantation of Abcg1(-/-) bone marrow cells resulted in a significant reduction in lesion size in both mouse models, despite the fact that lipid levels increased in the lung, spleen, and kidney [16].
• Male F1 New Zealand Black X New Zealand White mice, which spontaneously develop immune complex renal disease, underwent unilateral nephrectomy at 3 months of age and were compared with sham-operated controls [28].
• Ten male New Zealand White rabbits were transplanted with cardiac-aorta allografts from male Dutch Belted rabbits [29].
• Suppression of disease in New Zealand Black/New Zealand White lupus-prone mice by adoptive transfer of ex vivo expanded regulatory T cells [30].
• Orderly pattern of development of the autoantibody response in (New Zealand White x BXSB)F1 lupus mice: characterization of target antigens and antigen spreading by two-dimensional gel electrophoresis and mass spectrometry [31].

References