BIOMARKERS

Molecular Biopsy of Human Tumors

- a resource for Precision Medicine *

923 related articles for article (PubMed ID: 15301543)

  • 1. Substitutions of glutamate 110 and 111 in the middle helix 4 of human apolipoprotein A-I (apoA-I) by alanine affect the structure and in vitro functions of apoA-I and induce severe hypertriglyceridemia in apoA-I-deficient mice.
    Chroni A; Kan HY; Kypreos KE; Gorshkova IN; Shkodrani A; Zannis VI
    Biochemistry; 2004 Aug; 43(32):10442-57. PubMed ID: 15301543
    [TBL] [Abstract][Full Text] [Related]  

  • 2. 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.
    Chroni A; Kan HY; Shkodrani A; Liu T; Zannis VI
    Biochemistry; 2005 Mar; 44(10):4108-17. PubMed ID: 15751988
    [TBL] [Abstract][Full Text] [Related]  

  • 3. Pathway of biogenesis of apolipoprotein E-containing HDL in vivo with the participation of ABCA1 and LCAT.
    Kypreos KE; Zannis VI
    Biochem J; 2007 Apr; 403(2):359-67. PubMed ID: 17206937
    [TBL] [Abstract][Full Text] [Related]  

  • 4. 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.
    Koukos G; Chroni A; Duka A; Kardassis D; Zannis VI
    Biochem J; 2007 Aug; 406(1):167-74. PubMed ID: 17506726
    [TBL] [Abstract][Full Text] [Related]  

  • 5. LCAT can rescue the abnormal phenotype produced by the natural ApoA-I mutations (Leu141Arg)Pisa and (Leu159Arg)FIN.
    Koukos G; Chroni A; Duka A; Kardassis D; Zannis VI
    Biochemistry; 2007 Sep; 46(37):10713-21. PubMed ID: 17711302
    [TBL] [Abstract][Full Text] [Related]  

  • 6. ABCA1 promotes the de novo biogenesis of apolipoprotein CIII-containing HDL particles in vivo and modulates the severity of apolipoprotein CIII-induced hypertriglyceridemia.
    Kypreos KE
    Biochemistry; 2008 Sep; 47(39):10491-502. PubMed ID: 18767813
    [TBL] [Abstract][Full Text] [Related]  

  • 7. Role of apoA-I, ABCA1, LCAT, and SR-BI in the biogenesis of HDL.
    Zannis VI; Chroni A; Krieger M
    J Mol Med (Berl); 2006 Apr; 84(4):276-94. PubMed ID: 16501936
    [TBL] [Abstract][Full Text] [Related]  

  • 8. Residues Leu261, Trp264, and Phe265 account for apolipoprotein E-induced dyslipidemia and affect the formation of apolipoprotein E-containing high-density lipoprotein.
    Drosatos K; Kypreos KE; Zannis VI
    Biochemistry; 2007 Aug; 46(33):9645-53. PubMed ID: 17655277
    [TBL] [Abstract][Full Text] [Related]  

  • 9. Discrete roles of apoA-I and apoE in the biogenesis of HDL species: lessons learned from gene transfer studies in different mouse models.
    Zannis VI; Koukos G; Drosatos K; Vezeridis A; Zanni EE; Kypreos KE; Chroni A
    Ann Med; 2008; 40 Suppl 1():14-28. PubMed ID: 18246469
    [TBL] [Abstract][Full Text] [Related]  

  • 10. The carboxy-terminal region of apoA-I is required for the ABCA1-dependent formation of alpha-HDL but not prebeta-HDL particles in vivo.
    Chroni A; Koukos G; Duka A; Zannis VI
    Biochemistry; 2007 May; 46(19):5697-708. PubMed ID: 17447731
    [TBL] [Abstract][Full Text] [Related]  

  • 11. The 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.
    Chroni A; Liu T; Gorshkova I; Kan HY; Uehara Y; Von Eckardstein A; Zannis VI
    J Biol Chem; 2003 Feb; 278(9):6719-30. PubMed ID: 12488454
    [TBL] [Abstract][Full Text] [Related]  

  • 12. Dissociation of high density lipoprotein precursors from apolipoprotein B-containing lipoproteins in the presence of unesterified fatty acids and a source of apolipoprotein A-I.
    Musliner TA; Long MD; Forte TM; Nichols AV; Gong EL; Blanche PJ; Krauss RM
    J Lipid Res; 1991 Jun; 32(6):917-33. PubMed ID: 1940624
    [TBL] [Abstract][Full Text] [Related]  

  • 13. Trimerized apolipoprotein A-I (TripA) forms lipoproteins, activates lecithin: cholesterol acyltransferase, elicits lipid efflux, and is transported through aortic endothelial cells.
    Ohnsorg PM; Mary JL; Rohrer L; Pech M; Fingerle J; von Eckardstein A
    Biochim Biophys Acta; 2011 Dec; 1811(12):1115-23. PubMed ID: 21930241
    [TBL] [Abstract][Full Text] [Related]  

  • 14. Role of individual amino acids of apolipoprotein A-I in the activation of lecithin:cholesterol acyltransferase and in HDL rearrangements.
    Cho KH; Durbin DM; Jonas A
    J Lipid Res; 2001 Mar; 42(3):379-89. PubMed ID: 11254750
    [TBL] [Abstract][Full Text] [Related]  

  • 15. Probing the pathways of chylomicron and HDL metabolism using adenovirus-mediated gene transfer.
    Zannis VI; Chroni A; Kypreos KE; Kan HY; Cesar TB; Zanni EE; Kardassis D
    Curr Opin Lipidol; 2004 Apr; 15(2):151-66. PubMed ID: 15017358
    [TBL] [Abstract][Full Text] [Related]  

  • 16. Domains of apoE4 required for the biogenesis of apoE-containing HDL.
    Vezeridis AM; Chroni A; Zannis VI
    Ann Med; 2011 Jun; 43(4):302-11. PubMed ID: 21604997
    [TBL] [Abstract][Full Text] [Related]  

  • 17. ApoA-IV promotes the biogenesis of apoA-IV-containing HDL particles with the participation of ABCA1 and LCAT.
    Duka A; Fotakis P; Georgiadou D; Kateifides A; Tzavlaki K; von Eckardstein L; Stratikos E; Kardassis D; Zannis VI
    J Lipid Res; 2013 Jan; 54(1):107-15. PubMed ID: 23132909
    [TBL] [Abstract][Full Text] [Related]  

  • 18. Plasma levels of 27-hydroxycholesterol in humans and mice with monogenic disturbances of high density lipoprotein metabolism.
    Karuna R; Holleboom AG; Motazacker MM; Kuivenhoven JA; Frikke-Schmidt R; Tybjaerg-Hansen A; Georgopoulos S; van Eck M; van Berkel TJ; von Eckardstein A; Rentsch KM
    Atherosclerosis; 2011 Feb; 214(2):448-55. PubMed ID: 21130455
    [TBL] [Abstract][Full Text] [Related]  

  • 19. Effects of apoA-V on HDL and VLDL metabolism in APOC3 transgenic mice.
    Qu S; Perdomo G; Su D; D'Souza FM; Shachter NS; Dong HH
    J Lipid Res; 2007 Jul; 48(7):1476-87. PubMed ID: 17438339
    [TBL] [Abstract][Full Text] [Related]  

  • 20. Generation of a recombinant apolipoprotein E variant with improved biological functions: hydrophobic residues (LEU-261, TRP-264, PHE-265, LEU-268, VAL-269) of apoE can account for the apoE-induced hypertriglyceridemia.
    Kypreos KE; van Dijk KW; Havekes LM; Zannis VI
    J Biol Chem; 2005 Feb; 280(8):6276-84. PubMed ID: 15576362
    [TBL] [Abstract][Full Text] [Related]  

    [Next]    [New Search]
    of 47.