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SRP034009
Homo sapiens
6 Downloadable Samples
IlluminaHiSeq2000
Description
We evaluated the transcriptome changes induced by infection with Salmonella (20 hpi, MOI 100). Overall design: Transcriptmic profiles of HeLa cells infected with Salmonella Typhimurium were generated by deep sequencing, using Illumina HiSeq 2000.
Publication Title
Functional high-throughput screening identifies the miR-15 microRNA family as cellular restriction factors for Salmonella infection.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 5 Downloadable Samples
- IlluminaHiSeq2000
Description
We identified miRNAs differentially regulated upon Salmonella infection by comparative deep-sequencing analysis of cDNA libraries prepared from the small RNA population (10–29 nt) of HeLa cells infected with Salmonella (20 hpi) and mock-treated cells. Considering that at a MOI of 25 Salmonella is internalized in only 10-15% of the HeLa cells, we separated the fraction of cells which had internalized Salmonella (Salmonella+) from the bystander fraction (Salmonella-) by fluorescence-activated cell sorting (FACS), and extended the analysis of miRNA changes to these samples. Interestingly, we observed that Salmonella infection induces a significant decrease in the expression of all the detected members of the miR-15 family Overall design: miRNA profiles of HeLa cells infected with Salmonella Typhimurium were generated by deep sequencing, using Illumina HiSeq2000.
Publication Title
Functional high-throughput screening identifies the miR-15 microRNA family as cellular restriction factors for Salmonella infection.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaHiSeq2000
Description
To have a global picture of the targets of the miR-15 family, we assessed transcriptome changes, by deep-sequencing, of HeLa cells transfected with 3 members of the miR-15 family (miR-15a, miR-16 or miR-503) or a control miRNA (cel-miR-231). We observed a very extensive overlap between the genes down-regulated by these 3 miRNAs, as expected for miRNAs belonging to the same family. Overall design: transcriptmic profiles of HeLa cells treated miR-15a, miR-16, miR-503 and control-miR were generated by deep sequencing, using Illumina HiSeq2000.
Publication Title
Functional high-throughput screening identifies the miR-15 microRNA family as cellular restriction factors for Salmonella infection.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
We evaluated the transcriptome changes induced by infection of Hela 229 cells with Shigella flexneri. The sample set consists of a control (mock), total population of infected sample and infected sample sorted into Shigella positive and Shigella negative population. Overall design: Transcriptmic profiles of HeLa cells infected with Shigella were generated by high throughput sequencing using Illumina HiSeq2000.
Publication Title
Analysis of host microRNA function uncovers a role for miR-29b-2-5p in Shigella capture by filopodia.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 2 Downloadable Samples
- IlluminaHiSeq2000
Description
To have a global picture of the targets of the mir-29b-2-5p, we assessed transcriptome changes, by deep-sequencing, of HeLa cells transfected with this miRNA or a control miRNA (cel-miR-231). Overall design: Transcriptmic profiles of HeLa cells treated miR-29b-2-5p and control-miR were generated by deep sequencing, using Illumina HiSeq2000.
Publication Title
Analysis of host microRNA function uncovers a role for miR-29b-2-5p in Shigella capture by filopodia.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 18 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Biased GPCR agonists are orthosteric ligands that possess pathway-selective efficacy, activating or inhibiting only a subset of the signaling repertoire of their cognate receptors. In vitro, D-Trp12,Tyr34-bPTH(7-34) (PTH-{beta}arr), a biased agonist for the type 1 parathyroid hormone receptor, antagonizes receptor-G protein coupling but activates arrestin-dependent signaling. In vivo, both PTH-{beta}arr and the conventional agonist PTH(1-34) stimulate anabolic bone formation. To understand how two PTH1R ligands with markedly different in vitro efficacy could elicit similar in vivo responses, we analyzed transcriptional profiles from calvarial bone of mice treated for 8 weeks with vehicle, PTH-{beta}arr or PTH(1-34). Treatment of wild type mice with PTH-{beta}arr primarily affected pathways that promote expansion of the osteoblast pool, notably cell cycle regulation, cell survival and migration. These responses were absent in beta-arrestin2 null mice, identifying them as downstream targets of beta-arrestin2-mediated signaling. In contrast, PTH(1-34) primarily affected pathways classically associated with enhanced bone formation, including collagen synthesis and matrix mineralization. PTH(1-34) actions were less dependent on beta-arrestin2, as might be expected of a ligand capable of G protein activation. These results illustrate the uniqueness of biased agonism in vivo and demonstrate that functional selectivity can be exploited to change the quality of GPCR efficacy.
Publication Title
β-arrestin-selective G protein-coupled receptor agonists engender unique biological efficacy in vivo.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 23 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Rheumatoid arthritis (RA) is an inflammatory joint disorder that results in progressive joint damage when insufficiently treated. In order to prevent joint destruction and functional disability in RA, early diagnosis and initiation of appropriate treatment with Disease-Modifying Antirheumatic Drugs (DMARDs) is needed. However, in daily clinical practice, patients may initially display symptoms of arthritis that do not fulfil the classification criteria for a definite diagnosis of RA, or any other joint disease, a situation called Undifferentiated Arthritis (UA). Out of the patients with UA, 30 to 50% usually develop RA, and early identification of these remains a challenge.
Publication Title
Identification of distinct gene expression profiles in the synovium of patients with systemic lupus erythematosus.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Treatment
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
TNF antagonists are routinely used in severe rheumatoid arthritis (RA) patients who failed conventional DMARD therapy. According to large clinical trials, the three available drugs (adalimumab, infliximab and etanercept) display similar effects in terms of efficacy, tolerability and side effects. These studies also indicate that about 25% of RA patients treated with TNF-antagonists do not display any significant clinical improvement.
Publication Title
Gene expression profiling in the synovium identifies a predictive signature of absence of response to adalimumab therapy in rheumatoid arthritis.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
TNFalpha and IL1beta play a pathogenic role in rheumatoid arthritis. Both cytokines are known to activate cytokine and metalloproteinase secretion by synovial fibroblasts. In the present study, we wanted to investigate whether TNFalpha and IL1beta displayed differential effects on cultured Fibroblast-like Synovial Cells derived from RA patients. Global gene expression analyses indicated that both cytokines induced similar genes in these cells.
Publication Title
Gene expression profiling in the synovium identifies a predictive signature of absence of response to adalimumab therapy in rheumatoid arthritis.
Sample Metadata Fields
Specimen part, Disease, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- NextSeq 500
Description
There is a growing body of evidence about the presence and the activity of the miRISC in the nucleus of mammalian cells. Here, we show by quantitative proteomic analysis that Ago2 interacts with nucleoplasmic Sfpq in a RNA-dependent fashion. By HITS-CLIP and transcriptomic analyses, we demonstrated that Sfpq directly controls the miRNA targeting of a subset of crucial miRNA-target mRNAs when it binds locally. Sfpq modulates miRNA targeting in both nucleoplasm and cytoplasm, indicating a nucleoplasmic imprinting of Sfpq-target mRNAs that influence miRNA targeting in both cellular compartments. Mechanistically, Sfpq binds to a sizeable set of long 3'UTR forming long aggregates to optimize miRNA position/recruitment to selected binding sites, as we show for Lin28A mRNA. These results extend the miRNA-mediated post-transcriptional gene silencing into the nucleoplasm and indicate that an unique Sfpq-dependent post-transcriptional strategy for controlling both nuclear and cytoplasmic gene expression takes place in cells during physio-pathological events. Overall design: RNA-seq of P19 cells control and upon SFPQ knockdown both in triplicates
Publication Title
Post-transcriptional gene silencing mediated by microRNAs is controlled by nucleoplasmic Sfpq.
Sample Metadata Fields
Specimen part, Subject
View Samples