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Journal Abstract Search

132 related items for PubMed ID: 11116060

  • 1. Sphingomyelinase converts lipoproteins from apolipoprotein E knockout mice into potent inducers of macrophage foam cell formation.
    Marathe S, Choi Y, Leventhal AR, Tabas I.
    Arterioscler Thromb Vasc Biol; 2000 Dec; 20(12):2607-13. PubMed ID: 11116060
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  • 2. The distal pathway of lipoprotein-induced cholesterol esterification, but not sphingomyelinase-induced cholesterol esterification, is energy-dependent.
    Skiba PJ, Zha X, Maxfield FR, Schissel SL, Tabas I.
    J Biol Chem; 1996 Jun 07; 271(23):13392-400. PubMed ID: 8662777
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  • 3. Modification of type III VLDL, their remnants, and VLDL from ApoE-knockout mice by p-hydroxyphenylacetaldehyde, a product of myeloperoxidase activity, causes marked cholesteryl ester accumulation in macrophages.
    Whitman SC, Hazen SL, Miller DB, Hegele RA, Heinecke JW, Huff MW.
    Arterioscler Thromb Vasc Biol; 1999 May 07; 19(5):1238-49. PubMed ID: 10323775
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  • 4. The very low- and intermediate-density lipoprotein fraction isolated from apolipoprotein E-knockout mice transforms macrophages to foam cells through an apolipoprotein E-independent pathway.
    Hakamata H, Sakaguchi H, Zhang C, Sakashita N, Suzuki H, Miyazaki A, Takeya M, Takahashi K, Kitamura N, Horiuchi S.
    Biochemistry; 1998 Sep 29; 37(39):13720-7. PubMed ID: 9753460
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  • 5. Pitavastatin inhibits remnant lipoprotein-induced macrophage foam cell formation through ApoB48 receptor-dependent mechanism.
    Kawakami A, Tani M, Chiba T, Yui K, Shinozaki S, Nakajima K, Tanaka A, Shimokado K, Yoshida M.
    Arterioscler Thromb Vasc Biol; 2005 Feb 29; 25(2):424-9. PubMed ID: 15591219
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  • 6. Secretory sphingomyelinase, a product of the acid sphingomyelinase gene, can hydrolyze atherogenic lipoproteins at neutral pH. Implications for atherosclerotic lesion development.
    Schissel SL, Jiang X, Tweedie-Hardman J, Jeong T, Camejo EH, Najib J, Rapp JH, Williams KJ, Tabas I.
    J Biol Chem; 1998 Jan 30; 273(5):2738-46. PubMed ID: 9446580
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  • 7. Acid sphingomyelinase promotes lipoprotein retention within early atheromata and accelerates lesion progression.
    Devlin CM, Leventhal AR, Kuriakose G, Schuchman EH, Williams KJ, Tabas I.
    Arterioscler Thromb Vasc Biol; 2008 Oct 30; 28(10):1723-30. PubMed ID: 18669882
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  • 14. Uptake by J774 macrophages of very-low-density lipoproteins isolated from apoE-deficient mice is mediated by a distinct receptor and stimulated by lipoprotein lipase.
    Hendriks WL, van der Sman-de Beer F, van Vlijmen BJ, van Vark LC, Hofker MH, Havekes LM.
    Arterioscler Thromb Vasc Biol; 1997 Mar 30; 17(3):498-504. PubMed ID: 9102168
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  • 15. Cholesteryl ester accumulation in mouse peritoneal macrophages induced by beta-migrating very low density lipoproteins from patients with atypical dysbetalipoproteinemia.
    Bersot TP, Innerarity TL, Mahley RW, Havel RJ.
    J Clin Invest; 1983 Sep 30; 72(3):1024-33. PubMed ID: 6309903
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  • 16. Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis.
    Morita SY.
    Biol Pharm Bull; 2016 Sep 30; 39(1):1-24. PubMed ID: 26725424
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  • 17. Lipoprotein-antibody immune complexes. Their catabolism and role in foam cell formation.
    Klimov AN, Denisenko AD, Popov AV, Nagornev VA, Pleskov VM, Vinogradov AG, Denisenko TV, Magracheva EYa, Kheifes GM, Kuznetzov AS.
    Atherosclerosis; 1985 Dec 30; 58(1-3):1-15. PubMed ID: 4091875
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  • 18. Sphingomyelinase enhances low density lipoprotein uptake and ability to induce cholesteryl ester accumulation in macrophages.
    Xu XX, Tabas I.
    J Biol Chem; 1991 Dec 25; 266(36):24849-58. PubMed ID: 1761578
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