Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse neural stem cell lines overexpressing Nurr1 to clonal controls


ABSTRACT: The orphan nuclear receptor Nurr1 has been shown to be critical for the development of ventral midbrain dopaminergic neurons. Consequently, the development of ES cells overexpressing Nurr1 has raised hope for the development of cell replacement therapies for Parkinson's Disease to replace degenerated dopaminergic neurons. However, the molecular consequences of Nurr1 on gene expression in these cells remain unknown. To address this, stable, clonal, c17.2 neural stem cell lines were established that overexpressed the orphan nuclear receptor Nurr1 (clone 42 & clone 48) or parental control cell line (puroB & puroD, respectively). Experiment Overall Design: Stable neural stem cell lines were grown in proliferating conditions and matched for further microarray analysis based on their similar proliferation rates: Experiment Overall Design: clone 42(c42) vs. puroB(pB) Experiment Overall Design: clone 42(c48) vs. puroD(pD)

ORGANISM(S): Mus musculus

SUBMITTER: Kyle Matthew Sousa 

PROVIDER: E-GEOD-3571 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Microarray analyses support a role for Nurr1 in resistance to oxidative stress and neuronal differentiation in neural stem cells.

Sousa Kyle M KM   Mira Helena H   Hall Anita C AC   Jansson-Sjöstrand Lottie L   Kusakabe Moriaki M   Arenas Ernest E  

Stem cells (Dayton, Ohio) 20061012 2


Nurr1 is an orphan nuclear receptor required for the development of midbrain dopaminergic neurons. To better understand the molecular consequences of Nurr1 expression, we compared the transcriptomes of two independent control and Nurr1-expressing NSC lines using Affymetrix cDNA microarrays. These data reveal the regulation of genes involved in promoting cell survival (trophic/growth factors and stress response genes) and in preventing cell death (decreased caspase-3 and caspase-11 expression). W  ...[more]

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