To identify gene expression profile changes upon SNRNP40 depletion, RNA-sequencing was performed on breast cancer cells transfected with siRNAs targeting SNRNP40. Overall design: Libraries were generated using ScriptSeq v2 RNA-seq Library Preparation Kit (Epicentre) and run on Illumina HiSeq 2500.
Highly variable cancer subpopulations that exhibit enhanced transcriptome variability and metastatic fitness.
No sample metadata fields
View SamplesWe performed whole-genome stability measurements for MDA-MB-231 and its highly metastatic derivative MDA-LM2. Our goal was to identify post-transcriptonal regulons that are deregulated en route to higher metastatic capacity. Overall design: Cells were pulsed with 4-thiouridine for 2 hours and then RNA was extracted at 0, 2, 4, and 7 hr time-points in quadruplicate from each cell line. 4sU labeling followed by RNA-seq was then used to measure the abundance of transcripts in each population. A decay rate was estimated based on the rate at which transcript abundance was reduced at these time-points.
Metastasis-suppressor transcript destabilization through TARBP2 binding of mRNA hairpins.
Cell line, Subject, Time
View SamplesTo identify MBNL1-dependent changes in gene expression, MDA-MB-231 cells expressing either control or MBNL1-targeting shRNAs were transcriptomically profiled. Overall design: MDA-MB-231 cells stably expressing a control or two independent MBNL1-targeting shRNAs were sequenced in biological duplicate.
Muscleblind-like 1 suppresses breast cancer metastatic colonization and stabilizes metastasis suppressor transcripts.
No sample metadata fields
View SamplesWe used Illlumina Artseq Ribo Profile to perform ribosome footprinting on the above cell lines Overall design: We followed the manufacturer's protocol: Cells were treated with cycloheximide (0.1 mg/ml) to inhibit translation; total RNA and ribosome-protected RNA fragments were isolated and library preped for sequencing simultaneously.
Modulated Expression of Specific tRNAs Drives Gene Expression and Cancer Progression.
No sample metadata fields
View SamplesWe used Illlumina Artseq Ribo Profile to perform ribosome footprinting on the above cell lines Overall design: We followed the manufacturer's protocol: Cells were treated with cycloheximide (0.1 mg/ml) to inhibit translation; total RNA(tt) and ribosome-protected RNA fragments (RPF) were isolated and library preped for sequencing simultaneously.
Modulated Expression of Specific tRNAs Drives Gene Expression and Cancer Progression.
No sample metadata fields
View SamplesWe used Illlumina Artseq Ribo Profile to perform ribosome footprinting on the above cell lines Overall design: We followed the manufacturer's protocol: Cells were treated with cycloheximide (0.1 mg/ml) to inhibit translation; total RNA(tt) and ribosome-protected RNA fragments (RPF) were isolated and library preped for sequencing simultaneously.
Modulated Expression of Specific tRNAs Drives Gene Expression and Cancer Progression.
No sample metadata fields
View SamplesWe used Illlumina Artseq Ribo Profile to perform ribosome footprinting on the above cell lines Overall design: We followed the manufacturer's protocol: Cells were treated with cycloheximide (0.1 mg/ml) to inhibit translation; total RNA(tt) and ribosome-protected RNA fragments (RPF) were isolated and library preped for sequencing simultaneously.
Modulated Expression of Specific tRNAs Drives Gene Expression and Cancer Progression.
Cell line, Subject
View SamplesPurpose: We purified spinal cord microglia utilizing percoll gradients and magnetic beads, followed by transcriptome profiling (RNA-seq) to define microglia expression profiles against other neural, immune cell-types. We next observed how the microglai transcriptomes change during activation in the SOD1-G93A mouse model of motor neuron degeneration at 3 timepoints. We also compared these profiles with that induced by LPS injection. Results and conclusions: ALS microglia were found to differ substantially from those activated by LPS and from M1/M2 macrophages by comparison with published datasets. These ALS microglia showing substantial induction of a "neurodegeneration-tailored phenotype", with induction of lysosomal, RNA splicing, and Alzheimer''s disease pathway genes. Overall they express a mixture of neuroprotective and neurotoxic factors during activation in ALS mice, showing that neuro-immune activation in the spinal cord is a double-edged sword. We also detected the transcriptional nature of surface marker expression in microglia (CD11b, CD86, CD11c), and substantial T-cell microglia cross-talk using correlative microglia transcriptome/FACS analysis. Overall design: 42 total RNA samples from purified spinal cord microglia were subjected to paired-end RNA-sequencing. Parallel flow cytometry data was collected from the same spinal cords.
A neurodegeneration-specific gene-expression signature of acutely isolated microglia from an amyotrophic lateral sclerosis mouse model.
Specimen part, Disease, Disease stage, Subject
View SamplesA major role of NINJA is to repress root jasmonate signalling and allow normal cell elongation.
Multilayered Organization of Jasmonate Signalling in the Regulation of Root Growth.
Specimen part
View SamplesPurpose: To determine effects of arsenic on gene expression in polarized primary human bronchial epithelial (HBE) cells and impact on transcriptional response to Pseudomonas aeruginosa infection Methods: mRNA profiles of HBE cells from 6 donors exposed to 0, 5, 10 or 50 ug/L total arsenic +/- Pseudomonas aeruginosa (48 samples) were generated using Illumina sequencing, aligned in CLC Genomics workbench and analyzed for DE in EdgeR Findings: 20-30 million reads were mapped per sample and transcripts were identifed that were significantly differentially expressed in response to arsenic and Pseudomonas aeruginosa Overall design: Gene expression profiles of HBE cells from 6 donors exposed to three concentrations of arsenic +/- Pseudomonas were generated using mRNA sequencing
Arsenic alters transcriptional responses to Pseudomonas aeruginosa infection and decreases antimicrobial defense of human airway epithelial cells.
Sex, Specimen part, Subject
View Samples