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Maternal diabetes increases the risk of caudal regression caused by retinoic acid.
Reduced expression of pax-3 is associated with overexpression of cdc46 in the mouse embryo.
Diacylglycerol production and protein kinase C activity are increased in a mouse model of diabetic embryopathy.
Neural tube defects in embryos of diabetic mice: role of the Pax-3 gene and apoptosis.
Hypoxic stress in diabetic pregnancy contributes to impaired embryo gene expression and defective development by inducing oxidative stress.
AMP-activated protein kinase mediates effects of oxidative stress on embryo gene expression in a mouse model of diabetic embryopathy.
Activation of the hexosamine pathway causes oxidative stress and abnormal embryo gene expression: involvement in diabetic teratogenesis.
Oxidant regulation of gene expression and neural tube development: Insights gained from diabetic pregnancy on molecular causes of neural tube defects.
Evidence that elevated glucose causes altered gene expression, apoptosis, and neural tube defects in a mouse model of diabetic pregnancy.
Mice, Inbred ICR
Lack of metformin effect on mouse embryo AMPK activity: implications for metformin treatment during pregnancy.
Increased DNA methyltransferase 3b (Dnmt3b)-mediated CpG island methylation stimulated by oxidative stress inhibits expression of a gene required for neural tube and neural crest development in diabetic pregnancy.
Mice Inbred ICR