Antioxidant supplementation ameliorates molecular deficits in Smith-Lemli-Opitz syndrome. Korade Z, Xu L, Harrison FE, Ahsen R, Hart SE, Folkes OM, Mirnics K, Porter NA (2014) Biol Psychiatry 75: 215-22 DHCEO accumulation is a critical mediator of pathophysiology in a Smith-Lemli-Opitz syndrome model. Xu L, Mirnics K, Bowman AB, Liu W, Da J, Porter NA, Korade Z (2012) Neurobiol Dis 45: 923-9 Biological activities of 7-dehydrocholesterol-derived oxysterols: implications for Smith-Lemli-Opitz syndrome. Korade Z, Xu L, Shelton R, Porter NA (2010) J Lipid Res 51: 3259-69 An oxysterol biomarker for 7-dehydrocholesterol oxidation in cell/mouse models for Smith-Lemli-Opitz syndrome. Xu L, Korade Z, Rosado DA, Liu W, Lamberson CR, Porter NA (2011) J Lipid Res 52: 1222-33 Metabolism of oxysterols derived from nonenzymatic oxidation of 7-dehydrocholesterol in cells. Xu L, Korade Z, Rosado DA, Mirnics K, Porter NA (2013) J Lipid Res 54: 1135-43 Molecular consequences of altered neuronal cholesterol biosynthesis. Korade Z, Kenworthy AK, Mirnics K (2009) J Neurosci Res 87: 866-75 NRIF is a regulator of neuronal cholesterol biosynthesis genes. Korade Z, Kenchappa RS, Mirnics K, Carter BD (2009) J Mol Neurosci 38: 152-8 Behavioral and serotonergic response changes in the Dhcr7-HET mouse model of Smith-Lemli-Opitz syndrome. Korade Z, Folkes OM, Harrison FE (2013) Pharmacol Biochem Behav 106: 101-8
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