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Domains of apoE required for binding to apoE receptor 2 and to phospholipids: implications for the functions of apoE in the brainDNA binding specificity and transactivation properties of SREBP-2 bound to multiple sites on the human apoA-II promoterPoint mutations in apolipoprotein A-I mimic the phenotype observed in patients with classical lecithin:cholesterol acyltransferase deficiencyPurification and characterization of nuclear factors binding to the negative regulatory element D of human apolipoprotein A-II promoter: a negative regulatory effect is reversed by GABP, an Ets-related protein.Intracellular early and late modifications of human apolipoprotein A-II. Effect of glutamine- +1 to leucine substitution.Detailed molecular model of apolipoprotein A-I on the surface of high-density lipoproteins and its functional implications.Molecular etiology of a dominant form of type III hyperlipoproteinemia caused by R142C substitution in apoE4Murine mammary-derived cells secrete the N-terminal 41% of human apolipoprotein B on high density lipoprotein-sized lipoproteins containing a triacylglycerol-rich core.Domains of apoE4 required for the biogenesis of apoE-containing HDL.Alteration of negatively charged residues in the 89 to 99 domain of apoA-I affects lipid homeostasis and maturation of HDL.Inhibition of c-Jun-N-terminal kinase increases cardiac peroxisome proliferator-activated receptor alpha expression and fatty acid oxidation and prevents lipopolysaccharide-induced heart dysfunction.Probing the pathways of chylomicron and HDL metabolism using adenovirus-mediated gene transfer.A2b adenosine receptor regulates hyperlipidemia and atherosclerosisRole of apoA-I, ABCA1, LCAT, and SR-BI in the biogenesis of HDL.Allele-dependent thermodynamic and structural perturbations in ApoE variants associated with the correction of dyslipidemia and formation of spherical ApoE-containing HDL particles.The carboxy-terminal region of apoA-I is required for the ABCA1-dependent formation of alpha-HDL but not prebeta-HDL particles in vivo.Identification of the molecular target of small molecule inhibitors of HDL receptor SR-BI activity.Residues Leu261, Trp264, and Phe265 account for apolipoprotein E-induced dyslipidemia and affect the formation of apolipoprotein E-containing high-density lipoprotein.Isolation and characterization of the human apolipoprotein A-I gene.Intracellular and extracellular processing of human apolipoprotein A-I: secreted apolipoprotein A-I isoprotein 2 is a propeptide.Direct physical interactions between HNF-4 and Sp1 mediate synergistic transactivation of the apolipoprotein CIII promoter.Transactivation of the human apolipoprotein CII promoter by orphan and ligand-dependent nuclear receptors. The regulatory element CIIC is a thyroid hormone response element.Synergism between nuclear receptors bound to specific hormone response elements of the hepatic control region-1 and the proximal apolipoprotein C-II promoter mediate apolipoprotein C-II gene regulation by bile acids and retinoids.Binding specificity and modulation of the ApoA-I promoter activity by homo- and heterodimers of nuclear receptors.LCAT can rescue the abnormal phenotype produced by the natural ApoA-I mutations (Leu141Arg)Pisa and (Leu159Arg)FIN.Inflammatory signaling pathways regulating ApoE gene expression in macrophages.Naturally occurring and bioengineered apoA-I mutations that inhibit the conversion of discoidal to spherical HDL: the abnormal HDL phenotypes can be corrected by treatment with LCAT.Specific mutations in ABCA1 have discrete effects on ABCA1 function and lipid phenotypes both in vivo and in vitro.SR-BI mediates cholesterol efflux via its interactions with lipid-bound ApoE. Structural mutations in SR-BI diminish cholesterol efflux.An indirect negative autoregulatory mechanism involved in hepatocyte nuclear factor-1 gene expression.Deletions of helices 2 and 3 of human apoA-I are associated with severe dyslipidemia following adenovirus-mediated gene transfer in apoA-I-deficient mice.Contribution of the hormone-response elements of the proximal ApoA-I promoter, ApoCIII enhancer, and C/EBP binding site of the proximal ApoA-I promoter to the hepatic and intestinal expression of the ApoA-I and ApoCIII genes in transgenic mice.Regulatory gene mutations affecting apolipoprotein gene expression: functions and regulatory behavior of known genes may guide future pharmacogenomic approaches to therapy.Hyperlipidemia in APOE2 transgenic mice is ameliorated by a truncated apoE variant lacking the C-terminal domain.ABCA1 and amphipathic apolipoproteins form high-affinity molecular complexes required for cholesterol efflux.Functional specificity of two hormone response elements present on the human apoA-II promoter that bind retinoid X receptor alpha/thyroid receptor beta heterodimers for retinoids and thyroids: synergistic interactions between thyroid receptor beta aThe central helices of ApoA-I can promote ATP-binding cassette transporter A1 (ABCA1)-mediated lipid efflux. Amino acid residues 220-231 of the wild-type ApoA-I are required for lipid efflux in vitro and high density lipoprotein formation in vivo.Reconstituted discoidal ApoE-phospholipid particles are ligands for the scavenger receptor BI. The amino-terminal 1-165 domain of ApoE suffices for receptor binding.Transcriptional regulation of the genes involved in lipoprotein transport. The role of proximal promoters and long-range regulatory elements and factors in apolipoprotein gene regulation.Activation of CAAT enhancer-binding protein delta (C/EBPdelta) by interleukin-1 negatively influences apolipoprotein C-III expression.
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hulumtues
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wetenschapper
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հետազոտող
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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Vassilis I Zannis
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P106
P21
P31
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0000-0002-1295-7155