GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE90nnn/GSE90046/primaryOK2000000GenomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE90046GEOGSE0falseC/EBPβ deficiency reshapes microglial gene expressionCCAAT/enhancer binding protein β (C/EBPβ) is a transcription factor that regulates the expression of important pro-inflammatory genes in microglia. Mice deficient for C/EBPβ show protection against excitotoxic and ischemic CNS damage but the involvement of the various C/EBPβ expressing cell types in this neuroprotective effect is not solved. Since C/EBPβ-deficient microglia show attenuated neurotoxicity in culture we hypothesized that specific C/EBPβ deficiency in microglia could be neuroprotective in vivo. In this study we have tested this hypothesis by generating mice with myeloid C/EBPβ deficiency. Mice with myeloid C/EBPβ deficiency were generated by crossing LysMCre and C/EBPβfl/fl mice . Primary microglial cultures from C/EBPβfl/fl (named here as WT) and LysMCre-C/EBPβfl/fl (named here as KO) mice were treated with lipopolysaccharide ± interferon γ (IFNγ) for 6 h and gene expression was analyzed by RNA sequencing. LysMCre-C/EBPβfl/fl mice showed an efficiency of C/EBPβ deletion of 100% in cultured microglia. Transcriptomic analysis of C/EBPβ-deficient primary microglia revealed C/EBPβ-dependent expression of 1068 genes, significantly enriched in inflammatory and innate immune responses GO terms. This study provides new data that support a central role for C/EBPβ in the biology of activated microglia.2017/06/13GSE90046GSM2396050GSM2396061GSM2396062GSM2396051GSM2396052GSM2396063GSM2396053GSM2396064GSM2396060GSM2396058GSM2396069GSM2396059GSM2396049GSM2396065GSM2396054GSM2396055GSM2396066GSM2396067GSM2396056GSM2396068GSM239605711002SRP09362490046Mus musculus[28302135][30382133]