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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Animals, Chromatin Immunoprecipitation, Electrophysiology, Gene Expression Profiling, Gene Expression Regulation, Genotype, Hedgehog Proteins, Immunohistochemistry, Inflammation, Interferon-gamma, Mice, Mice, Inbred C57BL, Neural Stem Cells, Phenotype, STAT1 Transcription Factor, Signal Transduction, Stem Cells.
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Are interferon gamma and sonic hedgehog signaling required to dysregulate murine neural stem/precursor cells? Context: The pro-inflammatory cytokine interferon gamma (IFNγ), a key player in various neurological diseases, was recently shown to induce a dysregulated phenotype in neural stem/precursor cells (NSPCs) that is characterized by the simultaneous expression of glial and neuronal markers and irregular electrophysiological properties. Thus far, the mechanisms of this phenomenon have remained unclear. To determine if binding of the signal transducers and activators of transcription (Stat 1) to the sonic hedgehog (SHH) promoter is important for this phenomenon to occur, chromatin immunoprecipitation and pharmacological inhibition studies were performed. We report here that the activation of both the Stat 1 and SHH pathways is necessary to elicit the dysregulated phenotype.
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Thus, blocking these pathways might preserve functional differentiation of NSPCs under inflammatory conditions leading to more effective regeneration. Final Decision: yes