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2011
W. Zeng, Liu, L., Tong, Y., Liu, H. M., Dai, L., and Mao, M., A66G and C524T polymorphisms of the methionine synthase reductase gene are associated with congenital heart defects in the Chinese Han population, vol. 10, pp. 2597-2605, 2011.
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Hungarian cohort-controlled trial of periconceptional multivitamin supplementation shows a reduction in certain congenital abnormalities. Birth Defects Res. A Clin. Mol. Teratol. 70: 853-861. http://dx.doi.org/10.1002/bdra.20086 PMid:15523663 Deng L, Elmore CL, Lawrance AK, Matthews RG, et al. (2008). Methionine synthase reductase deficiency results in adverse reproductive outcomes and congenital heart defects in mice. Mol. Genet. Metab. 94: 336-342. http://dx.doi.org/10.1016/j.ymgme.2008.03.004 PMid:18413293    PMCid:3110750 Elmore CL, Wu X, Leclerc D, Watson ED, et al. (2007). Metabolic derangement of methionine and folate metabolism in mice deficient in methionine synthase reductase. Mol. Genet. Metab. 91: 85-97. http://dx.doi.org/10.1016/j.ymgme.2007.02.001 PMid:17369066    PMCid:1973089 Fredriksen A, Meyer K, Ueland PM, Vollset SE, et al. (2007). Large-scale population-based metabolic phenotyping of thirteen genetic polymorphisms related to one-carbon metabolism. Hum. Mutat. 28: 856-865. http://dx.doi.org/10.1002/humu.20522 PMid:17436311 Gellekink H, den Heijer M, Heil SG and Blom HJ (2005). Genetic determinants of plasma total homocysteine. Semin. Vasc. Med. 5: 98-109. http://dx.doi.org/10.1055/s-2005-872396 PMid:16047263 Hoffman JI and Kaplan S (2002). The incidence of congenital heart disease. J. Am. Coll. Cardiol. 39: 1890-1900. http://dx.doi.org/10.1016/S0735-1097(02)01886-7 Huhta JC, Linask K and Bailey L (2006). Recent advances in the prevention of congenital heart disease. Curr. Opin. Pediatr. 18: 484-489. http://dx.doi.org/10.1097/01.mop.0000245347.45336.d7 PMid:16969161 Itikala PR, Watkins ML, Mulinare J, Moore CA, et al. (2001). Maternal multivitamin use and orofacial clefts in offspring. Teratology 63: 79-86. http://dx.doi.org/10.1002/1096-9926(200102)63:2<79::AID-TERA1013>3.0.CO;2-3 Kapusta L, Haagmans ML, Steegers EA, Cuypers MH, et al. (1999). Congenital heart defects and maternal derangement of homocysteine metabolism. J. Pediatr. 135: 773-774. http://dx.doi.org/10.1016/S0022-3476(99)70102-2 Lai E (2001). Application of SNP technologies in medicine: lessons learned and future challenges. Genome Res. 11: 927- 929. http://dx.doi.org/10.1101/gr.192301 PMid:11381021 Leclerc D, Odievre M, Wu Q, Wilson A, et al. (1999). Molecular cloning, expression and physical mapping of the human methionine synthase reductase gene. Gene 240: 75-88. http://dx.doi.org/10.1016/S0378-1119(99)00431-X Olteanu H and Banerjee R (2001). Human methionine synthase reductase, a soluble P-450 reductase-like dual flavoprotein, is sufficient for NADPH-dependent methionine synthase activation. J. Biol. Chem. 276: 35558-35563. http://dx.doi.org/10.1074/jbc.M103707200 PMid:11466310 Rosenquist TH, Ratashak SA and Selhub J (1996). Homocysteine induces congenital defects of the heart and neural tube: effect of folic acid. Proc. Natl. Acad. Sci. U. S. A. 93: 15227-15232. http://dx.doi.org/10.1073/pnas.93.26.15227 Shaw GM, Lu W, Zhu H, Yang W, et al. (2009). 118 SNPs of folate-related genes and risks of spina bifida and conotruncal heart defects. BMC Med. Genet. 10: 49. http://dx.doi.org/10.1186/1471-2350-10-49 PMid:19493349    PMCid:2700092 Silaste ML, Rantala M, Sampi M, Alfthan G, et al. (2001). Polymorphisms of key enzymes in homocysteine metabolism affect diet responsiveness of plasma homocysteine in healthy women. J. Nutr. 131: 2643-2647. PMid:11584084 Swanson DA, Liu ML, Baker PJ, Garrett L, et al. (2001). Targeted disruption of the methionine synthase gene in mice. Mol. Cell. Biol. 21: 1058-1065. http://dx.doi.org/10.1128/MCB.21.4.1058-1065.2001 PMid:11158293    PMCid:99560 Tennstedt C, Chaoui R, Korner H and Dietel M (1999). Spectrum of congenital heart defects and extracardiac malformations associated with chromosomal abnormalities: results of a seven year necropsy study. Heart 82: 34-39. PMid:10377306    PMCid:1729082 Tierney BJ, Ho T, Reedy MV and Brauer PR (2004). Homocysteine inhibits cardiac neural crest cell formation and morphogenesis in vivo. Dev. Dyn. 229: 63-73. http://dx.doi.org/10.1002/dvdy.10469 PMid:14699578 van Beynum IM, Kouwenberg M, Kapusta L, den Heijer M, et al. (2006). MTRR 66A>G polymorphism in relation to congenital heart defects. Clin. Chem. Lab. Med. 44: 1317-1323. http://dx.doi.org/10.1515/CCLM.2006.254 PMid:17087642 Verkleij-Hagoort AC, Verlinde M, Ursem NT, Lindemans J, et al. (2006). Maternal hyperhomocysteinaemia is a risk factor for congenital heart disease. BJOG 113: 1412-1418. http://dx.doi.org/10.1111/j.1471-0528.2006.01109.x Verkleij-Hagoort AC, van Driel LM, Lindemans J, Isaacs A, et al. (2008). Genetic and lifestyle factors related to the periconception vitamin B12 status and congenital heart defects: a dutch case-control study. Mol. Genet. Metab. 94: 112-119. http://dx.doi.org/10.1016/j.ymgme.2007.12.002 PMid:18226574
C. L. Hou, Zhang, W., Wei, Y., Mi, J. H., Li, L., Zhou, Z. H., Zeng, W., and Ying, D. J., Zinc finger protein A20 overexpression inhibits monocyte homing and protects endothelial cells from injury induced by high glucose, vol. 10, pp. 1050-1059, 2011.
Fogelman AM, Elahi F, Sykes K, Van Lenten BJ, et al. (1988). Modification of the Recalde method for the isolation of human monocytes. J. Lipid Res. 29: 1243-1247. PMid:3183529 La Fontaine J, Harkless LB, Davis CE, Allen MA, et al. (2006). Current concepts in diabetic microvascular dysfunction. J. Am. Podiatr. Med. Assoc. 96: 245-252. PMid:16707637 Lutz J, Luong Le A, Strobl M, Deng M, et al. (2008). The A20 gene protects kidneys from ischaemia/reperfusion injury by suppressing pro-inflammatory activation. J. Mol. Med. 86: 1329-1339. doi:10.1007/s00109-008-0405-4 PMid:18813897 McGinn S, Saad S, Poronnik P and Pollock CA (2003). High glucose-mediated effects on endothelial cell proliferation occur via p38 MAP kinase. Am. J. Physiol. Endocrinol. Metab. 285: E708-E717. PMid:12783777 Mohan S, Mohan N, Valente AJ and Sprague EA (1999). Regulation of low shear flow-induced HAEC VCAM-1 expression and monocyte adhesion. Am. J. Physiol. 276: C1100-C1107. PMid:10329958 Patel VI, Daniel S, Longo CR, Shrikhande GV, et al. (2006). A20, a modulator of smooth muscle cell proliferation and apoptosis, prevents and induces regression of neointimal hyperplasia. FASEB J. 20: 1418-1430. doi:10.1096/fj.05-4981com PMid:16816117 Romero MJ, Platt DH, Tawfik HE, Labazi M, et al. (2008). Diabetes-induced coronary vascular dysfunction involves increased arginase activity. Circ. Res. 102: 95-102. doi:10.1161/CIRCRESAHA.107.155028 PMid:17967788    PMCid:2822539 Wang AB, Li HL, Zhang R, She ZG, et al. (2007). A20 attenuates vascular smooth muscle cell proliferation and migration through blocking PI3k/Akt singling in vitro and in vivo. J. Biomed. Sci. 14: 357-371. doi:10.1007/s11373-007-9150-x PMid:17260188 Yang WS, Seo JW, Han NJ, Choi J, et al. (2008). High glucose-induced NF-kappaB activation occurs via tyrosine phosphorylation of IkappaBalpha in human glomerular endothelial cells: involvement of Syk tyrosine kinase. Am. J. Physiol. Renal Physiol. 294: F1065-F1075. doi:10.1152/ajprenal.00381.2007 PMid:18353872 Zeng W, Li L, Yuan W, Wei Y, et al. (2009). A20 overexpression inhibits low shear flow-induced CD14-positive monocyte recruitment to endothelial cells. Biorheology 46: 21-30. PMid:19252225 Zhu CH, Ying DJ, Mi JH, Zhang W, et al. (2004). The zinc finger protein A20 protects endothelial cells from burns serum injury. Burns 30: 127-133. doi:10.1016/j.burns.2003.08.010 PMid:15019119