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Abstract NURR1 is a member of the nuclear receptor superfamily of transcription factors and plays an essential role in development and maintenance of midbrain dopaminergic neurons. Reduced NURR1 expression is associated with Parkinson’s disease and drug addiction. Expression-level dependent effects of NURR1 on gene expression have been studied, but biological pathways that are expression-level specific have not been examined. In order to better understand the biological processes and pathways that are dependent on the NURR1 expression level, genome-wide gene expression data under three different NURR1 expression levels were downloaded from the NCBI Gene Expression Omnibus repository (accession number GSE33434) and analyzed with KEGG signaling pathways. Significantly impacted biological pathways by NURR1 expression level were identified. Inhibition of the immune/pro-inflammatory process was observed only under low NURR1 expression, whereas high NURR1 expression led to inhibition of the cell proliferation process and activation of the immune response. Inhibition of dopamine synthesis and activation of synaptic plasticity were continuously maintained from low to high NURR1 expression level. Taken together, low expression of NURR1 seemed to make cells flexible to changes like neuronal development by inhibiting the immune response, whereas high expression of NURR1 seemed to maintain neuronal status of cells by inhibiting the cell cycle and activating the immune response.
BioChip Journal – Springer Journals
Published: Jun 1, 2014
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