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SRP122966
Mus musculus
35 Downloadable Samples
Illumina HiSeq 2500
Description
Our study looks at the dirsruption of lung circadian transcriptome that occurs when neutrophils are depleted (by application of antibodies (anti-Ly6G-1A8) to wildtype C57BL/6 mice, or Diphtheria toxin (DT) to neutrophil-specific DT-susceptible mice (MRP8-Cre;iDTR-flox)). Overall design: Lungs were harvested from neutrophil-depleted (antibody or DT) or non-depleted mice, in normal light-controlled mouse facility (ZT4) or 12h inverted light cabinets (ZT16). Experiments were carried out over 3 batches (July 2017, September 2017, and April 2018), with 3 or 4 mice per group. Antibody-depleted and non-depleted mice were tested for the July 2017 and September 2017 batches, whereas DT-depleted mice were tested only in April 2018.
Publication Title
Neutrophils instruct homeostatic and pathological states in naive tissues.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Mus musculus
- 14 Downloadable Samples
- Illumina HiSeq 2500
Description
Our study aims to analyze time-dependent changes in neutrophil phenotype, compare them with included neutrophil-specific mutants, and indentify common signatures among the 5 groups Overall design: Blood neutrophils from wild-type and mutants were isolated based on Ly6G staining, then standard RNA extraction procedures were performed. Wild-type samples were extracted at ZT5 and ZT13, all other samples at ZT5.
Publication Title
A Neutrophil Timer Coordinates Immune Defense and Vascular Protection.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 5 Downloadable Samples
- Illumina HiSeq 2500
Description
Our study aims to analyze time-dependent changes in neutrophil phenotype Overall design: Blood neutrophils were isolated based on Ly6G staining, then standard RNA extraction procedures were performed. This samples were extracted at ZT13.
Publication Title
A Neutrophil Timer Coordinates Immune Defense and Vascular Protection.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 9 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip
Description
Inhibition of the costimulatory CD40-CD40L receptor/ligand dyad drastically reduces atherosclerosis. However, its long-term blockage can result in immune suppression. We recently identified small molecule inhibitors that block the interaction between CD40 and TNF Receptor Associated Factor (TRAF) 6 (TRAF-STOPs), while leaving CD40-TRAF2/3/5 interactions intact, thereby preserving CD40-mediated immunity. Here we further characterized the working mechanisms of TRAF-STOPs 6877002 and 6860766 in atherogenesis.
Publication Title
Targeting CD40-Induced TRAF6 Signaling in Macrophages Reduces Atherosclerosis.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Heterogeneity, shortage of material, and lack of progenitor-specific cell surface markers are major obstacles to elucidating the mechanisms underlying developmental processes. Here we report a proteomic platform that alleviates these difficulties and demonstrate its effectiveness in fractionating heterogeneous cultures of early endoderm derived from human embryonic stem cells. The approach, designated cell-capture antibody array, is based on highly parallel, comparative screening of live cell populations using hundreds of antibodies directed against cell-surface antigens. The results demonstrate the potential of the cell-capture antibody array as a powerful tool for detailed dissection of heterogeneous cellular systems.
Publication Title
Proteomics-based dissection of human endoderm progenitors by differential cell capture on antibody array.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
A functional interaction between peroxisome proliferator-activated receptor alpha (PPARalpha) and components of the circadian clock has been suggested; however, it remains to be clarified whether those transcriptional factors interact with each other to regulate the expression of their target genes.
Publication Title
Bezafibrate induces plasminogen activator inhibitor-1 gene expression in a CLOCK-dependent circadian manner.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
Transcriptional responses to stimuli are regulated by tuning rates of transcript production and degradation. Here we show that stimulation-induced changes in transcript production and degradation rates can be inferred from simultaneously measured precursor mRNA (pre-mRNA) and mature mRNA profiles. Our studies on the transcriptome-wide responses to extracellular stimuli in different cellular model systems revealed hitherto unanticipated dynamics of transcript production and degradation rates. Intriguingly, genes with similar mRNA profiles often exhibit marked differences in the amplitude and onset of their production. Moreover, we identify a group of genes, which take advantage of the unexpectedly large dynamic range of production rates to expedite their induction by a transient production overshoot. These findings provide an unprecedented quantitative view on processes governing transcriptional responses, and may have broad implications for understanding their regulation at the transcriptional and post-transcriptional levels.
Publication Title
Coupled pre-mRNA and mRNA dynamics unveil operational strategies underlying transcriptional responses to stimuli.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations have shown a dramatic response to EGFR inhibitors (EGFR-TKI). EGFR T790M mutation and MET amplification have been recognized as major mechanisms of acquired resistance to EGFR-TKI. Therefore, MET inhibitors have recently been used in NSCLC patients in clinical trials. In this study, we tried to identify the mechanism of acquired resistance to MET inhibitor. We analyzed the antitumor effects of two MET inhibitors, PHA-665752 and crizotinib, in 10 NSCLC cell lines. EBC1 cells with MET amplification were the only cells that were sensitive to both MET inhibitors. We established PHA-665752-resistant EBC1 cells, namely EBC1-R cells. EBC1-R cells showed overexpression of ATP-binding cassette sub-family B member 1 (ABCB1) as well as phosphorylation of MET. EBC1-R cells grew as cell spheres that exhibited cancer stem cell-like (CSC) properties and epithelial mesenchymal transition (EMT). The levels of two miRNAs, miR-374a and miR-138 which targeted ABCB1, were decreased in EBC1-R cells. ABCB1 siRNA and ABCB1 inhibitor elacridar could reduce sphere numbers and suppress EMT. Elacridar could also reverse the resistance to PHA-665752 in EBC1-R cells. Our study demonstrated that ABCB1 overexpression which was associated with CSC properties and EMT was involved in the acquired resistance to MET inhibitor. Inhibition of ABCB1 might be a novel therapeutic strategy for NSCLC patients with acquired resistance to MET inhibitor.
Publication Title
Inhibition of ABCB1 Overcomes Cancer Stem Cell-like Properties and Acquired Resistance to MET Inhibitors in Non-Small Cell Lung Cancer.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- IlluminaHiSeq2500
Description
The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-?B subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-?B p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-?B-dependent enhancers in epithelial cells. Overall design: RNA-seq of KB cells either untreated or treated with IL-1 alpha
Publication Title
The Activation of IL-1-Induced Enhancers Depends on TAK1 Kinase Activity and NF-κB p65.
Sample Metadata Fields
No sample metadata fields
View Samples- Pan troglodytes, Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Gene expression study of human and Chimpanzee iPS cell.
Publication Title
New type of Sendai virus vector provides transgene-free iPS cells derived from chimpanzee blood.
Sample Metadata Fields
Specimen part
View Samples