Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice.
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Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids SignalingPhysiological and pathological roles of tissue plasminogen activator and its inhibitor neuroserpin in the nervous systemRegulation of DNA methylation by ethanol induces tissue plasminogen activator expression in astrocytesGenetic absence of nNOS worsens fetal alcohol effects in mice. I: behavioral deficits.Molecular pathways underpinning ethanol-induced neurodegeneration.Glia and neurodevelopment: focus on fetal alcohol spectrum disorders.Genetic absence of nNOS worsens fetal alcohol effects in mice. II: microencephaly and neuronal lossesImportance of genetics in fetal alcohol effects: null mutation of the nNOS gene worsens alcohol-induced cerebellar neuronal losses and behavioral deficits.Fetal alcohol exposure leads to abnormal olfactory bulb development and impaired odor discrimination in adult mice.CB1-receptor knockout neonatal mice are protected against ethanol-induced impairments of DNMT1, DNMT3A, and DNA methylation.The neuronal nitric oxide synthase (nNOS) gene and neuroprotection against alcohol toxicityEpiphyseal chondrocyte secondary ossification centers require thyroid hormone activation of Indian hedgehog and osterix signalingPostnatal ethanol exposure alters levels of 2-arachidonylglycerol-metabolizing enzymes and pharmacological inhibition of monoacylglycerol lipase does not cause neurodegeneration in neonatal mice.Passenger mutations and aberrant gene expression in congenic tissue plasminogen activator-deficient mouse strains.DNA modifications in models of alcohol use disorders.Effects of Ethanol on Brain Extracellular Matrix: Implications for Alcohol Use Disorder.A single day of 5-azacytidine exposure during development induces neurodegeneration in neonatal mice and neurobehavioral deficits in adult mice.Effects of long-term moderate ethanol and cholesterol on cognition, cholinergic neurons, inflammation, and vascular impairment in rats.Effects of Prenatal Alcohol Exposure (PAE): Insights into FASD using PAE Mouse Models.Fibrinolysis: from blood to the brain.CB1R-Mediated Activation of Caspase-3 Causes Epigenetic and Neurobehavioral Abnormalities in Postnatal Ethanol-Exposed Mice.
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P2860
Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice.
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2011 nî lūn-bûn
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2011 թուականի Մարտին հրատարակուած գիտական յօդուած
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2011 թվականի մարտին հրատարակված գիտական հոդված
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2011年の論文
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2011年論文
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2011年論文
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2011年論文
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2011年論文
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2011年論文
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2011年论文
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name
Tissue plasminogen activator i ...... etal alcohol syndrome in mice.
@ast
Tissue plasminogen activator i ...... etal alcohol syndrome in mice.
@en
Tissue plasminogen activator i ...... etal alcohol syndrome in mice.
@nl
type
label
Tissue plasminogen activator i ...... etal alcohol syndrome in mice.
@ast
Tissue plasminogen activator i ...... etal alcohol syndrome in mice.
@en
Tissue plasminogen activator i ...... etal alcohol syndrome in mice.
@nl
prefLabel
Tissue plasminogen activator i ...... etal alcohol syndrome in mice.
@ast
Tissue plasminogen activator i ...... etal alcohol syndrome in mice.
@en
Tissue plasminogen activator i ...... etal alcohol syndrome in mice.
@nl
P2860
P356
P1476
Tissue plasminogen activator i ...... fetal alcohol syndrome in mice
@en
P2093
Melissa Noel
P2860
P304
P356
10.1073/PNAS.1017608108
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P577
2011-03-07T00:00:00Z