Filters
Technology
Platform
E-MEXP-558
Mus musculus
6 Downloadable Samples
Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Effect of the ablation of connexin 30 in the stria vascularis
Publication Title
Connexin30 deficiency causes instrastrial fluid-blood barrier disruption within the cochlear stria vascularis.
Sample Metadata Fields
Age, Specimen part, Disease, Time
View Samples- Homo sapiens
- 27 Downloadable Samples
Illumina HiSeq 3000
Description
We recently reported that single-cell derived isogenic subclones of SKMEL5 cells have differential initial sensitivity to BRAF-inhibitors. In order to probe differences among these subclones, we selected three subclones with unique drug responses: progressing (SK-MEL-5 SC10), stationary (SK-MEL-5 SC07), and regressing (SK-MEL-5 SC01) and performed RNASeq. This study examines differentially expressed genes (DEGs) among the subclones to identify the molecular basis for initial differences in drug sensitivity. Overall design: Transcriptomics analysis between single-cell derived isogenic subclones of BRAF-mutated melanoma cell line, SK-MEL-5
Publication Title
A Nonquiescent "Idling" Population State in Drug-Treated, BRAF-Mutated Melanoma.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Promoter hypermethylation and transcriptional silencing is a common epigenetic mechanism of tumour suppressor inactivation in cancer, including malignant brain tumours.
Publication Title
Epigenetic genome-wide analysis identifies BEX1 as a candidate tumour suppressor gene in paediatric intracranial ependymoma.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Comparison of gene expression profile of Ewing sarcoma cells which have an exchange of the endogenous EWS/FLI1 to either wild-type or a turnover-deficient mutant EWS/FLI1. Most target genes are saturated as only a few target genes are soly driven by increasing protein amount.
Publication Title
Proteasomal Degradation of the EWS-FLI1 Fusion Protein Is Regulated by a Single Lysine Residue.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
In this study we could show that the treatment of primary murine prostate cancer(PCa) cells derived from the well-established TRAMP (transgenic adenocarcinoma ofmouse prostate) model with the histone deacetylase inhibitor (HDI) valproic acid (VPA) has an anti-proliferative, anti-migrative and anti-invasive effect on the cells.To our knowledge this is the first study that identified that treatment of PCa cells with VPA leads to the re-expression of cyclin D2, which is known to be frequently inactive in patients with PCa. Additionally, we could demonstrate that VPA specifically induces re-expression of cyclin D2 as a family member of the highly conserved Dtype cyclins in human colorectal and mammary gland adenocarcinoma cell lines, whereas VPA treatment has no effect in NIH/3T3 fibroblasts. The observed cyclin D2 re-expression in cancer cells is activated by an increase of histone acetylation in the promoter region of the cyclin D2 gene and might be the underlying molecular mechanism of the inhibition of proliferation of cancer cells after VPA treatment. Taken together, our results confirm VPA as an anticancer therapeutic option in tumors with epigenetically repressed cyclin D2 expression.
Publication Title
Valproic acid inhibits the proliferation of cancer cells by re-expressing cyclin D2.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 57 Downloadable Samples
- Illumina HiSeq 2500
Description
RNA-seq analysis from young and pre-glaucomatous DBA/2J retinal ganglion cells and control (age and sex-matched, D2-Gpnmb+) retinal ganglion cells Overall design: Retinal ganglion cell mRNA from 4 month (young) and 9 month (pre-glaucomatous) DBA/2J mice and age and sex-matched D2-Gpnmb+ controls
Publication Title
Nicotinamide and WLD<sup>S</sup> Act Together to Prevent Neurodegeneration in Glaucoma.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Our group recently described a population of antigen presenting cells that appear to be critical in psoriasis pathogenesis, termed inflammatory myeloid dendritic cells (CD11c+ BDCA1-). Triggering receptor expressed on myeloid cells type-1 (TREM-1) signaling was a major canonical pathway in the published transcriptome of these cells. TREM-1 is a member of the immunoglobulin superfamily, active through the DAP12 signaling pathway, with an unknown ligand. Activation through TREM-1 induces inflammatory cytokines including IL-8, MCP/CCL2 and TNF. We now show that TREM-1 was expressed in the skin of healthy and psoriatic patients, and there was increased soluble TREM-1 in the circulation of psoriasis patients. In psoriasis lesions, TREM-1 was co-localized with dendritic cells as well as CD31+ endothelial cells. TREM-1 expression was reduced with successful NB-UVB, etanercept and anti-IL-17 treatments. An in vitro model of PGN-activated monocytes as inflammatory myeloid DCs was developed to study TREM-1 blockade, and treatment with a TREM-1 blocking chimera decreased allogeneic Th17 activation, as well as IL-17 production. Furthermore, TREM-1 blockade of ex vivo psoriatic dendritic cells in an alloMLR also showed a decrease in IL-17. Together, these data suggest that the TREM-1 signaling pathway offers a novel therapeutic target to prevent the effects of inflammatory myeloid DCs in psoriasis.
Publication Title
TREM-1 as a potential therapeutic target in psoriasis.
Sample Metadata Fields
Specimen part
View Samples- Sus scrofa
- 83 Downloadable Samples
- Illumina HiSeq 2000
Description
Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) infection of 3rd trimester pregnant pigs can result in transmission of the virus to the fetus and ultimately death in utero or postnatally. Little is known about the immune response to infection at the maternal-fetal interface and in the fetus itself, or the molecular events behind virus transmission and disease progression in the fetus. To investigate these processes, RNA-sequencing of two tissues, uterine endothelium adjacent to the umbilical attachment site and fetal thymus, was performed 21 days post challenge on four groups of fetuses selected from a large PRRSV challenge experiment of pregnant gilts. Overall design: RNA-seq experiment compared gene expression between four different groups of fetuses (n=12 per group): control (CON-uninfected fetuses from mock inoculated gilts), UNINF (uninfected fetuses from PRRSV-inoculated gilts), INF (infected fetuses from PRRSV-inoculated gilts), and meconium-stained fetuses (MEC-meconium-stained fetuses from PRRSV-inoculated gilts) and investigated two tissues: uterine endometrium (with adherent placental tissue) at the site of umbilical attachment and fetal thymus (96 samples in total). Three contrasts were performed for the differential expression (edgeR) and network (WGCNA) analyses: UNINF v CON, INF v UNINF, and MEC v INF.
Publication Title
Genome-wide analysis of the transcriptional response to porcine reproductive and respiratory syndrome virus infection at the maternal/fetal interface and in the fetus.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 59 Downloadable Samples
- Illumina HiSeq 2000
Description
The RNA exosome is fundamental for the degradation of RNA in eukaryotic nuclei. Substrate targeting is facilitated by its co-factor Mtr4p/hMTR4, which links to RNA-binding protein adaptors. One such activity is the human Nuclear EXosome Targeting (NEXT) complex, composed of hMTR4, the Zn-finger protein ZCCHC8 and the RNA-binding factor RBM7. NEXT primarily targets early and unprocessed transcripts, demanding a rationale for how the nuclear exosome recognizes processed RNAs. Here, we describe the PolyA tail eXosome Targeting (PAXT) connection, comprising the hitherto uncharacterized ZFC3H1 Zn-knuckle protein as a central link between hMTR4 and the nuclear polyA binding protein PABPN1. Individual depletion of ZFC3H1 and PABPN1 results in the accumulation of common transcripts, that are generally both longer and more 3'polyadenylated than NEXT substrates. Importantly, ZFC3H1/PABPN1 and ZCCHC8/RBM7 contact hMTR4 in a mutually exclusive manner, revealing that the exosome targets nuclear transcripts of different maturation status by substituting its hMTR4-associating adaptors. Overall design: RNA from HeLa cells was analysed by next generation sequencing upon depletion of EGFP(control), RRP40, RBM7, ZCCHC8, PABPN1 and ZFC3H1. Both total and BrU RNA (one hour labeling) were collected for each condition in triplicates. The spike-in sequences used in the samples can be provided upon request.
Publication Title
Characterizing ZC3H18, a Multi-domain Protein at the Interface of RNA Production and Destruction Decisions.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 35 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
The aim of this study was to investigate the molecular mechanisms implicated in this mouse model of nemaline myopathy, and to further compare the molecular disease response in different skeletal muscles. For this purpose, snap frozen skeletla muscle specimens from wild type and transgenic for alpha tropomyosin slow mice were studied. Five different muscle types were used (diaphragm, plantaris, extensor digitorum longus, tibialis anterior, gastrocnemus). Mice were sacrificed between 7 and 10 months. RNA pools from 3-5 animals were created and each pool was hybridized to a U74Av2 Affymetrix GeneChip. Datasets from 36 GeneChips were included in this study.
Publication Title
Skeletal muscle repair in a mouse model of nemaline myopathy.
Sample Metadata Fields
No sample metadata fields
View Samples