Induction of embryonic dysmorphogenesis by high glucose concentration, disturbed inositol metabolism, and inhibited protein kinase C activity.
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Modeling anterior development in mice: diet as modulator of risk for neural tube defectsMaternal diabetes alters transcriptional programs in the developing embryo.Maternal dietary glycemic intake and the risk of neural tube defectsGene-environment interactions, folate metabolism and the embryonic nervous system.Protein kinase Cβ2 inhibition reduces hyperglycemia-induced neural tube defects through suppression of a caspase 8-triggered apoptotic pathway.Diabetic embryopathy: a role for the epigenome?Decoding the oxidative stress hypothesis in diabetic embryopathy through proapoptotic kinase signaling.The essential role of protein kinase Cδ in diabetes-induced neural tube defectsDiabetic embryopathy: studies using a rat embryo culture system and an animal model.Advances in understanding the molecular causes of diabetes-induced birth defects.Experimental mechanisms of diabetic embryopathy and strategies for developing therapeutic interventions.New concepts in diabetic embryopathyThe status of diabetic embryopathy.Acephalous lamb from an in vitro-produced sheep embryo.Alterations in methylation and expression levels of imprinted genes H19 and Igf2 in the fetuses of diabetic miceResponses of the embryonic epigenome to maternal diabetesDiabetic uterus environment may play a key role in alterations of DNA methylation of several imprinted genes at mid-gestation in mice.The "Other" Inositols and Their Phosphates: Synthesis, Biology, and Medicine (with Recent Advances in myo-Inositol Chemistry).Management of Type 2 diabetes and pregnancy.Genetic basis of susceptibility to teratogen induced birth defects.Intrauterine growth retardation in experimental diabetes: possible role of the placenta.Cardiac malformations are associated with altered expression of vascular endothelial growth factor and endothelial nitric oxide synthase genes in embryos of diabetic mice.Nitroxide radicals protect cultured rat embryos and yolk sacs from diabetic-induced damage.
P2860
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P2860
Induction of embryonic dysmorphogenesis by high glucose concentration, disturbed inositol metabolism, and inhibited protein kinase C activity.
description
2001 nî lūn-bûn
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2001年の論文
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2001年学术文章
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2001年学术文章
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2001年学术文章
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2001年学术文章
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2001年学术文章
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2001年學術文章
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name
Induction of embryonic dysmorp ...... ted protein kinase C activity.
@en
Induction of embryonic dysmorp ...... ted protein kinase C activity.
@nl
type
label
Induction of embryonic dysmorp ...... ted protein kinase C activity.
@en
Induction of embryonic dysmorp ...... ted protein kinase C activity.
@nl
prefLabel
Induction of embryonic dysmorp ...... ted protein kinase C activity.
@en
Induction of embryonic dysmorp ...... ted protein kinase C activity.
@nl
P2093
P2860
P356
P1476
Induction of embryonic dysmorp ...... ted protein kinase C activity.
@en
P2093
C R Wentzel
M B Gäreskog
U J Eriksson
P2860
P304
P356
10.1002/TERA.1034
P577
2001-05-01T00:00:00Z