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Comparison of GFP- and Nurr1-infected ES-cell derived neurons

ABSTRACT: ES cell-derived neurons of forebrain identity were isolated by magnetic sorting, cultured for 7 days and transduced with either Nurr1 or eGFP lentivirus. After an additional 12 h in culture, mRNA was isolated and subjected to microarray analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE20392 | GEO | 2010/06/01

SECONDARY ACCESSION(S): PRJNA125519

REPOSITORIES: GEO

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Comparison of GFP- and Nurr1-infected ES-cell derived neurons

Project description:ES cell-derived neurons of forebrain identity were isolated by magnetic sorting, cultured for 7 days and transduced with either Nurr1 or eGFP lentivirus. After an additional 12 h in culture, mRNA was isolated and subjected to microarray analysis. The raw data have been provided in CEL format The processed data have been provided in CHP format ES-cell derived forebrain neurons were plated in 10cm dishes and infected with either GFP or Nurr1 lentivirus at a MOI of 10. 18h after infection, RNA was prepped by the Qiagen mini kit and submitted to labeling and hybridization. Microarray experiments were carried out using GeneChip 430A 2.0 arrays (Affymetrix). Data was normalized and expression values were computed using the gcrma method. Statistical analysis was performed by empirical Bayes inference for linear models using the limma package. The inclusion criteria fold-change was > 1.6 and P < 0.001

2010-06-08 | E-GEOD-20392 | biostudies-arrayexpress

Adeno-associated virus (AAV) 9-mediated gene delivery of Nurr1 and Foxa2 cures symptoms and pathologies of Alzheimer disease model mice by suppressing neuro-inflammation and glial pathology.

Project description:In this study, AAV9-Nurr1 and AAV9-Foxa2 (or AAV9-Control as sham-operated control) were injected to hippocampus of 15-18 months old 3xTg Alzheimer's disease mice. And mouse hippocampal glia were primarily cultured at postnatal day 1 and forced expression of Nurr1 and Foxa2 with lentivirus (or lenti-Control).

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NURR1 activation in skeletal muscle controls systemic energy homeostasis (ChIP-seq)

Project description:Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1 and transgenic overexpression of NURR1 in skeletal muscle confers an endurance phenotype in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.

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