Transgenic mice engineered to target Cre/loxP-mediated DNA recombination into catecholaminergic neurons.
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An Efficient and Versatile System for Visualization and Genetic Modification of Dopaminergic Neurons in Transgenic MiceDepletion of canonical Wnt signaling components has a neuroprotective effect on midbrain dopaminergic neurons in an MPTP-induced mouse model of Parkinson's diseaseTh-MYCN mice with caspase-8 deficiency develop advanced neuroblastoma with bone marrow metastasis.New mouse lines for the analysis of neuronal morphology using CreER(T)/loxP-directed sparse labeling.Identification of neuronal enhancers of the proopiomelanocortin gene by transgenic mouse analysis and phylogenetic footprintingExpression by midbrain dopamine neurons of Sema3A and 3F receptors is associated with chemorepulsion in vitro but a mild in vivo phenotype.Spatial and temporal lineage analysis of a Pitx3-driven Cre-recombinase knock-in mouse model.The estrogen receptor α colocalizes with proopiomelanocortin in hypothalamic neurons and binds to a conserved motif present in the neuron-specific enhancer nPE2A 3.7 kb fragment of the mouse Scn10a gene promoter directs neural crest but not placodal lineage EGFP expression in a transgenic animal.Heterogeneous transgene expression in the retinas of the TH-RFP, TH-Cre, TH-BAC-Cre and DAT-Cre mouse lines.Selection of embryonic stem cell-derived enhanced green fluorescent protein-positive dopamine neurons using the tyrosine hydroxylase promoter is confounded by reporter gene expression in immature cell populations.Parkinson's disease: genetic versus toxin-induced rodent models.Molecular anatomy of the gut-brain axis revealed with transgenic technologies: implications in metabolic research.Atg5- and Atg7-dependent autophagy in dopaminergic neurons regulates cellular and behavioral responses to morphine.The nuclear transcription factor CREB: involvement in addiction, deletion models and looking forward.Transgenic expression of Cre recombinase from the tyrosine hydroxylase locus.The dopamine D4 receptor is essential for hyperactivity and impaired behavioral inhibition in a mouse model of attention deficit/hyperactivity disorder.Brain catecholamine depletion and motor impairment in a Th knock-in mouse with type B tyrosine hydroxylase deficiency.Neonatal 6-OHDA lesion model in mouse induces Attention-Deficit/ Hyperactivity Disorder (ADHD)-like behaviourErbB4 deletion in noradrenergic neurons in the locus coeruleus induces mania-like behavior via elevated catecholamines
P2860
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P2860
Transgenic mice engineered to target Cre/loxP-mediated DNA recombination into catecholaminergic neurons.
description
2003 nî lūn-bûn
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2003年の論文
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name
Transgenic mice engineered to ...... nto catecholaminergic neurons.
@en
Transgenic mice engineered to ...... nto catecholaminergic neurons.
@nl
type
label
Transgenic mice engineered to ...... nto catecholaminergic neurons.
@en
Transgenic mice engineered to ...... nto catecholaminergic neurons.
@nl
prefLabel
Transgenic mice engineered to ...... nto catecholaminergic neurons.
@en
Transgenic mice engineered to ...... nto catecholaminergic neurons.
@nl
P2093
P2860
P356
P1433
P1476
Transgenic mice engineered to ...... nto catecholaminergic neurons.
@en
P2093
Daniela Noaín
Diego M Gelman
M Elena Avale
Malcolm J Low
Marcelo Rubinstein
Verónica Otero
P2860
P304
P356
10.1002/GENE.10217
P577
2003-08-01T00:00:00Z