[1] Plump AS, Smith JD, Hayek T, et al.Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombinetion in ES Cells[J]. Cell , 1992, 71(10):343-353. [2] Christian M, Cermak T, Doyle EL, et al.Targeting DNA double-strand breaks with TAL effector nucleases[J]. Genetics, 2010, 186(2):757-761. [3] Urnov FD, Rebar EJ, Holmes MC, et al.Genome editing with engineered zinc finger nucleases[J]. Nat RevGenet, 2010, 11(9):636-646. [4] Miller JC, Tan S, Qiao G, et al.A TALE nuclease architecture for efficient genome editing[J]. Nat Biotechnol, 2011, 29(2): 143-148. [5] Mahfouz MM, Li L, Shamimuzzaman M, et al.De novo-engineered transcription activator-like effector (TALE) hybrid nuclease with novel DNA binding specificity creates double-strand breaks[J]. Proc Natl Acad Sci U S A, 2011, 108(6):2623-2628. [6] Breslow JL.Mouse models of atherosclerosis[J]. Science, 1996, 272(5262):685-688. [7] 刘雪梅, 吴符火. 几类高脂血症动物模型的比较[J] . 中西医结合学报, 2004, 2(2):132-134. [8] Zheng S, Geghman K, Shenoy S, et al.Retake the center stagenew development of rat genetics[J]. Genet Genomics, 2012, 39(6):261-268. [9] Zhang SH, Reddick RL, Piedrahita JA, et al.Spontaneous hypercholesterolemia and arterial lesions in mice lacking aopolipoprotein E[J]. Science, 1992, 258(10):468-471. [10] Mahfouz MM, Li L, Shamimuzzaman M, et al.De novo-engineered transcription activator-like effector (TALE) hybrid nuclease with novel DNA binding specificity creates double-strand breaks[J]. Proc Natl Acad Sci U S A, 2011, 108(6): 2623-2628. [11] Boch J, Scholze H, Schornack S, et al.Breaking the code of DNA binding specificity of TAL-type III effectors[J]. Science, 2009, 326(5959):1509-1512. [12] Moscou MJ, Bogdanove AJ.A simple cipher governs DNA recognition by TAL effectors[J]. Science, 2009, 326(5959): 1501. [13] Tesson L, Usal C, Menoret S, et al.Knockout rats generated by embryo microinjection of TALENs[J]. Nat Biotechnol, 2011, 29(8):695-696. [14] 邹移海, 陈嘉, 谢玲玲, 等. 实验性大鼠血脂检测[J] . 实验动物科学与管理, 2004, 21(1):4-5. [15] 施新猷. 医用实验动物学[M]. 北京: 人民军医出版社, 1999:388. [16] Yin K, Liao DF, Tang CK.ATP-binding membrane cassettetransporterA1 (ABCA1): a possible link between inflammation and reverse cholesterol transport[J]. Mol Med, 2010, 16(9-10):438-449. [17] Joyce C, Freeman L, Brewer HB, et al.Study of ABCA1 function in transgenic mice[J]. Arterioscler Thromb Vasc Biol, 2003, 23(6):965-971. [18] Van Eck M, Singaraja RR, Ye D, et al.Macrophage ATP-binding cassette transporter A1 overexpression inhibits atherosclerotic lesion progression in low-density lipo-protein receptor knockout mice[J]. Arterioscler Thromb Vasc Biol, 2006, 26(4):929-934. [19] Coutinho JM, Singaraja RR, Kang M, et al.Complete functional rescue of the ABCA-/- mouse by human BAC transgenesis[J]. J Lipid Res, 2005, 46(1):113-123. [20] van Eck M, Bos IS, Kaminski WE, et al. Leukocyte ABCA1 control susceptibility to atherosclerosis and macrophage recruitment into tissues[J]. Proc Natl Acad Sci U S A, 2002, 99(6):298-303. [21] Zhao Y, Pennings M, Hildebrand RB, et al.Enhanced foam cell formation, atherosclerotic lesion development, and inflammation by combined deletion of ABCA1 and SR-BI in bone marrow-derived cells in LDL receptor knockout mice on western-type diet[J]. Circ Res, 2010, 107(12):e20-31. [22] Out R, Hoekstra M, Habets K, et al.Combined deletion of macrophage ABCA1 and ABCG1 leads to massive lipid accumulation in tissue macrophages and distinct atherosclerosis at relatively low plasma cholesterol levels[J]. Arteioscler Thromb Vasc Biol, 2008, 28(2):258-264. |