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GSE31714
Mus musculus
8 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Mutations in the inner nuclear membrane protein emerin cause muscular dystrophy. Current evidence suggests that the muscle wasting is related to defects in muscle progenitor cell differentiation and regeneration. We obtained miRNA and mRNA expression data from wildtype and emerin-null cells and looked at gene expression differences between them.
Publication Title
Loss of emerin alters myogenic signaling and miRNA expression in mouse myogenic progenitors.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 34 Downloadable Samples
Illumina HiScanSQ
Description
RNA sequencing was performed on proliferating and differentiating wildtype and emerin-null myogenic progenitors to identify molecular pathways implicated in Emery-Dreifuss Muscular Dystrophy. Overall design: Total RNA was isolated from 2 million wildtype or emerin-null H2Ks during proliferation and at each day of differentiation using the miRNeasy Mini Kit (Qiagen, product #217004) and processed according to manufacturer's protocol. RNA was isolated from three independent cell culture plates for each sample.
Publication Title
Expression Profiling of Differentiating Emerin-Null Myogenic Progenitor Identifies Molecular Pathways Implicated in Their Impaired Differentiation.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Arabidopsis thaliana
- 12 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Aims: To determine the changes in the Arabidopsis axillary bud transcriptome in response to changes in the red light (R) to far red light (FR) ratio (R:FR).
Publication Title
Abscisic acid regulates axillary bud outgrowth responses to the ratio of red to far-red light.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
Different from canonical ubiquitin-like proteins, Hub1 does not form covalent conjugates with substrates but binds proteins non-covalently. In Saccharomyces cerevisiae, Hub1 associates with spliceosomes and mediates alternative splicing of SRC1, without affecting pre-mRNA splicing generally. Human Hub1 is highly similar to its yeast homolog, but its cellular function remains largely unexplored. Here, we show that human Hub1 binds to the spliceosomal protein Snu66 as in yeast, however, unlike its S. cerevisiae homolog, human Hub1 is essential for viability. Prolonged in vivo depletion of human Hub1 leads to various cellular defects, including splicing speckle abnormalities, partial nuclear retention of mRNAs, mitotic catastrophe and consequently cell death by apoptosis. Early consequences of Hub1 depletion are severe splicing defects, however, only for specific splice sites leading to exon skipping and intron retention. Thus, the ubiquitin-like protein Hub1 is not a canonical spliceosomal factor needed generally for splicing, but rather a modulator of spliceosome performance and facilitator of alternative splicing.
Publication Title
The conserved ubiquitin-like protein Hub1 plays a critical role in splicing in human cells.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 89 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
PBMC from house dust mite (HDM) sensitized atopics were cultured in the presence or absence of HDM extract for 24 hours.
Publication Title
Distinguishing benign from pathologic TH2 immunity in atopic children.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 144 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
PBMC from house dust mite (HDM) sensitized atopics with or without asthma (or nonallergic controls) were cultured in the presence or absence of HDM extract for 24 hours.
Publication Title
Differential gene network analysis for the identification of asthma-associated therapeutic targets in allergen-specific T-helper memory responses.
Sample Metadata Fields
Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 18 Downloadable Samples
- NextSeq 500
Description
BACKGROUND: Streptococcus pneumoniae, the pneumococcus, is the main etiological agent of pneumonia. Pneumococcal infection is initiated by bacterial adherence to lung epithelial cells. The exact transcriptional changes occurring in both host and microbe during infection are unknown. Here, we developed a time-resolved infection model of human lung alveolar epithelial cells by S. pneumoniae and assess the resulting transcriptome changes in both organisms simultaneously by using dual RNA-seq. RESULTS: Functional analysis of the time-resolved dual RNA-seq data identifies several features of pneumococcal infection. For instance, we show that the glutathione-dependent reactive oxygen detoxification pathway in epithelial cells is activated by reactive oxygen species produced by S. pneumoniae. Addition of the antioxidant resveratrol during infection abates this response. At the same time, pneumococci activate the competence regulon during co-incubation with lung epithelial cells. By comparing transcriptional changes between wild-type encapsulated and mutant unencapsulated pneumococci, we demonstrate that adherent pneumococci, but not free-floating bacteria, repress innate immune responses in epithelial cells including expression of the chemokine IL-8 and the production of antimicrobial peptides. We also show that pneumococci activate several sugar transporters in response to adherence to epithelial cells and demonstrate that this activation depends on host-derived mucins. CONCLUSIONS: We provide a dual-transcriptomics overview of early pneumococcal infection in a time-resolved manner, providing new insights into host-microbe interactions. To allow easy access to the data by the community, a web-based platform was developed ( http://dualrnaseq.molgenrug.nl ). Further database exploration may expand our understanding of epithelial-pneumococcal interaction, leading to novel antimicrobial strategies. Overall design: 5 time points are analysed (0, 30, 60, 120 and 240 minutes after infection). Each time point has two biological replicates except for the 240 mpi. Furthermore, each time point has two pneumococcal strains used to infect A549 cells, encapsulated and unencapsulated pneumococci. In total there are 18 samples. cellular infection model, contains rRNA-depleted total RNA from A549 epithelial cells and D39 S. pneumoniae
Publication Title
Time-resolved dual RNA-seq reveals extensive rewiring of lung epithelial and pneumococcal transcriptomes during early infection.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus, Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Analysis of expression profiles of human pDC cell line (CAL1) compared to an immature T cell line (MOLT4)
Publication Title
Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Analysis of expression profiles of pDCs from wild type and heterozygous E2-2 mice. Results show the control by E2-2 of the expression of pDC-enriched genes.
Publication Title
Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 35 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
In this randomised placebo-controlled trial, irritable bowel syndrome (IBS) patients were treated with faecal material from a healthy donor (n=8, allogenic FMT) or with their own faecal microbiota (n=8, autologous FMT). The faecal transplant was administered by whole colonoscopy into the caecum (30 g of stool in 150 ml sterile saline). Two weeks before the FMT (baseline) as well as two and eight weeks after the FMT, the participants underwent a sigmoidoscopy, and biopsies were collected at a standardised location (20-25 cm from the anal verge at the crossing with the arteria iliaca communis) from an uncleansed sigmoid. In patients treated with allogenic FMT, predominantly immune response-related genes sets were induced, with the strongest response two weeks after FMT. In patients treated with autologous FMT, predominantly metabolism-related gene sets were affected.
Publication Title
Allogenic Faecal Microbiota Transfer Induces Immune-Related Gene Sets in the Colon Mucosa of Patients with Irritable Bowel Syndrome.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples