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SRP093624
Mus musculus
21 Downloadable Samples
Illumina Genome Analyzer IIx
Description
CCAAT/enhancer binding protein ß (C/EBPß) is a transcription factor that regulates the expression of important pro-inflammatory genes in microglia. Mice deficient for C/EBPß show protection against excitotoxic and ischemic CNS damage but the involvement of the various C/EBPß expressing cell types in this neuroprotective effect is not solved. Since C/EBPß-deficient microglia show attenuated neurotoxicity in culture we hypothesized that specific C/EBPß deficiency in microglia could be neuroprotective in vivo. In this study we have tested this hypothesis by generating mice with myeloid C/EBPß deficiency. Mice with myeloid C/EBPß deficiency were generated by crossing LysMCre and C/EBPßfl/fl mice . Primary microglial cultures from C/EBPßfl/fl (named here as WT) and LysMCre-C/EBPßfl/fl (named here as KO) mice were treated with lipopolysaccharide ± interferon ? (IFN?) for 6 h and gene expression was analyzed by RNA sequencing. LysMCre-C/EBPßfl/fl mice showed an efficiency of C/EBPß deletion of 100% in cultured microglia. Transcriptomic analysis of C/EBPß-deficient primary microglia revealed C/EBPß-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/EBPß in the biology of activated microglia. Overall design: LysMCre-C/EBPßfl/fl genotype (12 samples): 4 samples treated with LPS, 4 with LPS +IFNg, and 4 vehicle. C/EBPßfl/fl genotype (9 samples): 3 samples treated with LPS, 3 with LPS +IFNg, and 3 vehicle. Design Case (Treatment LPS or LPS +INF) control (No treatment or vehicle) in LysMCre-C/EBPßfl/fl genotype and in C/EBPßfl/fl genotype
Publication Title
RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 64 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Temporally restricted feeding is known to impact the circadian clock. This dataset shows the effects of temporally restricted feeding on the hepatic transcriptome.
Publication Title
Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Restricted feeding impacts the hepatic circadian clock of WT mice. Cry1, Cry2 double KO mice lack a circadian clock and are thus expected to show rhythmical gene expression in the liver. Imposing a temporally restricted feeding schedule on these mice shows how the hepatic circadian clock and rhythmic food intake regulate rhythmic transcription in parallel
Publication Title
Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Temporally restricted feeding has a profound effect on the circadian clock. Fasting and feeding paradigms are known to influence hepatic transcription. This dataset shows the dynamic effects of refeeding mice after a 24hour fasting period.
Publication Title
Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 48 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
High-temporal resolution profiling was performed on mouse liver to detect rhythmic transcripts
Publication Title
Harmonics of circadian gene transcription in mammals.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 47 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
High-temporal resolution profiling was performed on NIH3T3 fibroblasts to detect rhythmic transcripts
Publication Title
Harmonics of circadian gene transcription in mammals.
Sample Metadata Fields
No sample metadata fields
View Samples- Staphylococcus aureus
- 6 Downloadable Samples
- Affymetrix S. aureus Genome Array (saureus)
Description
AFN-1252 is an inhibitor of fatty acid biosynthesis. Gene expression profiles were generated by microarray analysis of S. aureus cells following treatment with AFN-1252, an inhibitor of fatty acid synthesis.
Publication Title
Perturbation of Staphylococcus aureus gene expression by the enoyl-acyl carrier protein reductase inhibitor AFN-1252.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus, Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Quantitative assays for human DNA and mRNA were used to examine the paradox that intravenously (IV) infused human multipotent stromal cells (hMSCs) can enhance tissue repair without significant engraftment. After 2 X 106 hMSCs were IV infused into mice, most of the cells were trapped as emboli in lung. The cells in lung disappeared with a half-life of about 24 hr but < 1,000 cells appeared in 6 other tissues. The hMSCs in lung up-regulated expression of multiple genes with a large increase in the anti-inflammatory protein TSG-6. After myocardial infarction, IV hMSCs but not hMSCs transduced with TSG-6 siRNA decreased inflammatory responses, reduced infarct size, and improved cardiac function. IV administration of recombinant TSG-6 also reduced inflammatory responses and reduced infarct size. The results suggest improvements in animal models and patients after IV infusions of MSCs are at least in part explained by activation of MSCs to secrete TSG-6.
Publication Title
Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
We recently reported the discovery of a small molecule inhibitor, AI-10-49 which can specially inhibit the protein-protein interaction between RUNX1 tumor suppressor and CBFß-SMMHC oncogene. We also demonstrated that AI-10-49 can re-establish the RUNX1 transcriptional program in inv(16) cells and can extend the survival of inv(16) leukemic mice. To identify the transcriptional changes associated with AI-10-49, we performed RNA-seq analysis in ME-1 cells [human inv(16) leukemia cell line] treated with AI-10-49. Overall design: ME-1 cells were treated with DMSO/ AI-10-49 (1uM) for six hours, followed by RNA isolation. RNA libraries were sequenced using 90bp paired end reads on an Illumina HiSeqTM 2000.Three independent experiments were conducted for DMSO as well as AI-10-49 treatments.
Publication Title
CBFβ-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples