Purpose: Examine the effect of the long non-coding RNA PARROT on the transcriptome in HeLa cells. Overall design: Total RNA-seq of RNA from cells treated with the control knock-down (NK) or depleted of ENST00000046668 (PARROT) with two different siRNAs (si1 and si2) for 24h.
The long non-coding RNA PARROT is an upstream regulator of c-Myc and affects proliferation and translation.
No sample metadata fields
View SamplesWe used IMR90 ER:RAS cells infected with an empty vector or an shRNA for ARID1B and induced senescence by addition of 4OHT. 6 days later RNA was collected for gene expression analysis. With a functional screen we previously identified ARID1B as a new regulator of cellular senescence. By performing gene expression analysis we confirmed this finding and showed that knockdown of ARID1B prevents the expression of genes induced during senescence.
SWI/SNF regulates a transcriptional program that induces senescence to prevent liver cancer.
Cell line
View SamplesTo identify systemic cytokine patterns in Chronic Graft-versus-Host-Disease (CGVHD), we profiled the gene expression of circulating monocytes. Pathway analysis identified two gene sets that were significantly upregulated across a broad range of patients with inflammatory and sclerotic presentations: (1) genes induced by Type I and Type II IFN, and (2) receptor genes for innate immune responses to cellular damage. Multiple IFN-inducible genes involved in signal transduction, anti-viral function, lymphocyte homeostasis, trafficking, and antigen presentation were increased. Furthermore, upregulation of TLR/NLR/CLR receptor genes for nucleic acids, ribonucleoproteins and annexin implicated response to damaged cells as a source of activation of inflammasomes and induction of Type I IFN.
Upregulation of IFN-Inducible and Damage-Response Pathways in Chronic Graft-versus-Host Disease.
Specimen part, Disease
View SamplesRegeneration of transgenic cells remains a major obstacle to research and commercial deployment of transgenic plants for most species.
Genome scale transcriptome analysis of shoot organogenesis in Populus.
Sex
View SamplesExpression profile of human donor lungs that have developed primary graft dysfunction (PGD) after lung transplantation and those that have not.
Expression profiling of human donor lungs to understand primary graft dysfunction after lung transplantation.
No sample metadata fields
View SamplesPeripheral arterial disease (PAD) is a relatively common manifestation of systemic atherosclerosis that leads to progressive narrowing of the lumen of leg arteries. Circulating monocytes are in contact with the arterial wall and can serve as reporters of vascular pathology in the setting of PAD. We performed gene expression analysis of peripheral blood mononuclear cells (PBMC) in patients with PAD and controls without PAD to identify differentially regulated genes. We identified 87 genes differentially expressed in the setting of PAD; 40 genes were upregulated and 47 genes were downregulated. We employed an integrated bioinformatics pipeline coupled with literature curation to characterize the functional coherence of differentially regulated genes. Notably, upregulated genes mediate immune response, inflammation, apoptosis, stress response, phosphorylation, hemostasis, platelet activation and platelet aggregation. Downregulated genes included several genes from the zinc finger family that are involved in transcriptional regulation. These results provide insights into molecular mechanisms relevant to the pathophysiology of PAD.
Gene expression profiling of peripheral blood mononuclear cells in the setting of peripheral arterial disease.
Specimen part, Disease, Disease stage
View SamplesGene expression profiling to determine transcriptome changes following Snail or Slug expression in MCF-7 breast cancer cells
The transcription factors Snail and Slug activate the transforming growth factor-beta signaling pathway in breast cancer.
Cell line, Treatment
View SamplesSmall RNAs were deep sequenced from the liver and spleen of adult mice in an effort to identify somatic piRNAs. Following sequencing of all small RNAs, known non-coding RNAs were computationally removed from the dataset. The remaining RNAs were then mapped to the genome and analyzed for sequence characteristics (5'' base, length) typical of known piRNAs. To determine if any of the identified small RNAs were MIWI2 dependent, we deep sequenced small RNAs from liver and spleen of MIWI2 KO mice and analyzed them as above. Overall design: We deep sequenced small RNAs from the liver and spleen of one WT mouse and one MIWI2 knock-out mouse. We then trimmed sequencing adapters and removed known ncRNAs (rRNA, tRNA, snoRNA, snRNA, miRNA) from the dataset before aligning reads to the mm9 assembly of the mouse genome.
piRNA-like small RNAs mark extended 3'UTRs present in germ and somatic cells.
Specimen part, Cell line, Subject
View SamplesRNA-sequencing was conducted to profile the transcriptome of the post-ischemic mouse cortex at multiple reperfusion time-points. RNA was isolated from sham and middle cerebral artery occlusion (MCAO)-operated mice at different reperfusion time points (6 h, 12 h or 24 h; three independent biological replicates per group), converted into cDNA libraries, and used for Illumina deep sequencing on a NexSeq500 instrument. The sequencing reads that passed quality filters were analyzed at the transcript isoform level based on the Tuxedo software package. On average 40.6 million reads were obtained from each sample and genome mapping was on average 82.9% for all samples. We detected 20,748 genes and 56,586 isoforms in the sham group; 22,192 genes and 60,023 isoforms in the 6 h group; 21,771 genes and 59,539 isoforms in the 12 h group; and 21,576 genes and 59,020 isoforms in the 24 h group. Our study represents the first detailed analysis of post-stroke mouse cortex transcriptomes generated using RNA-sequencing technology. Overall design: Genome-wide transcriptomic profiles of healthy and post-ischemic mouse cortices at various reperfusion time-points (6 h, 12 h, or 24 h) were generated using Illumina sequencing.
Deep Sequencing Reveals Uncharted Isoform Heterogeneity of the Protein-Coding Transcriptome in Cerebral Ischemia.
Sex, Age, Specimen part, Cell line, Subject, Time
View SamplesPurpose:We have the first-reported set of glial-specific transcripts utilizing the Ribotag model. We use this model to explore glial changes in DNBS-induced inflammation and neurokinin-2 receptor (NK2R) antagonism. Methods: Actively translated mRNA profiles of the distal colon myeneteric plexi of Rpl22(+/-)Sox10(+/-) male and female mice 8-10 weeks old were obtained utilizing the HA-tagged ribosomal immunoprecipitation and downstream RNA extraction. Samples meeting RNA quality standards by 18S and 28S rRNA peaks by 2100 Bioanalyzer and RNA 6000 Nano LabChip Kit (Agilent) were deep sequenced with the Illumina HiSeq 4000. Results: We mapped approximately 30-50 millions reads per sample to the mouse genome (v88) and identified approximately 100K ribosome-associated transcripts, with Tuxedo workflow, in distal colon glial cells with DNBS-induced inflammation and NK2R antagonism and their respective controls. Of these transcripts, changes in biological processes associated with inflammation and other important enteric nervous system communications between samples have been identified. Conclusions: Our study demonstrates the first use of the Ribotag model to provide glial cell-specific actively-translated mRNA changes in DNBS-induced inflammation with and without functional NK2R signalling. Overall design: Distal colon glial mRNA samples from Ribotag Rpl22(+/-)Sox10(+/-) mice administered either saline or DNBS and DMSO vehicle or NK2R antagonism.
Communication Between Enteric Neurons, Glia, and Nociceptors Underlies the Effects of Tachykinins on Neuroinflammation.
Sex, Specimen part, Cell line, Subject
View Samples