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E-MEXP-1287
Drosophila melanogaster
4 Downloadable Samples
Affymetrix Drosophila Genome Array (drosgenome1)
Description
Effect of injury and Pseudomonas aeruginosa inoculation in Drosophila melanogaster
Publication Title
Involvement of skeletal muscle gene regulatory network in susceptibility to wound infection following trauma.
Sample Metadata Fields
Sex, Time
View Samples- Mus musculus
- 2 Downloadable Samples
Illumina HiSeq 2000
Description
Notch signaling critically controls cell fate decisions in mammals, both during embryogenesis and in adults. In the skeleton, Notch suppresses osteoblast differentiation and sustains bone marrow mesenchymal progenitors during postnatal life. Stabilizing mutations of Notch2 cause the Hajdu-Cheney syndrome characterized by early onset osteoporosis in humans, but the mechanism whereby Notch inhibits bone accretion is not fully understood.To gain further insights about the mechanism we performed RNA-seq experiments with the doxycycline-inducible NICD2-ST2 cells with or without doxycycline treatment for 24 hrs.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 5 Downloadable Samples
- IlluminaHiSeq2500
Description
we characterized the small RNA content of exosomes derived from gastric cancer cell lines by deep sequencing
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 95 Downloadable Samples
- Illumina HiSeq 2000
Description
We use single cell RNA-seq method to analysis the transcriptional heterogeneity in squamous cell carcinoma of urinary bladder. The single cell sequencing approach is based on the method of single-cell tagged reverse transcription (STRT).
Publication Title
No associated publication
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Macrophages from RA synovial fluids were compared to primary human monocyte-derived macrophages.
Publication Title
Interferon-γ Represses M2 Gene Expression in Human Macrophages by Disassembling Enhancers Bound by the Transcription Factor MAF.
Sample Metadata Fields
Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Gene expression analysis of freshly isolated CD14+ human monocytes and monocytes cultured in the presence or absence of interferon (IFN) -gamma for 24 h and then stimulated with Pam3Cys, a Toll-like receptor (TLR) 2 ligand, for 6 h. Results provide insight into mechanisms by which IFN-gamma reprograms early macrophage differentiation and subsequent response to TLR ligands.
Publication Title
Integrated regulation of Toll-like receptor responses by Notch and interferon-gamma pathways.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Complement receptor 2negative (CR2/CD21) B cells have been found enriched in patients with autoimmune diseases and in common variable immunodeficiency (CVID) patients who are prone to autoimmunity. However, the physiology of CD21/lo B cells remains poorly characterized. We found that some rheumatoid arthritis (RA) patients also display an increased frequency of CD21/lo B cells in their blood. A majority of CD21/lo B cells from RA and CVID patients expressed germline autoreactive antibodies, which recognized nuclear and cytoplasmic structures. In addition, these B cells were unable to induce calcium flux, become activated, or proliferate in response to B-cell receptor and/or CD40 triggering, suggesting that these autoreactive B cells may be anergic. Moreover, gene array analyses of CD21/lo B cells revealed molecules specifically expressed in these B cells and that are likely to induce their unresponsive stage. Thus, CD21/lo B cells contain mostly autoreactive unresponsive clones, which express a specific set of molecules that may represent new biomarkers to identify anergic B cells in humans.
Publication Title
Complement receptor 2/CD21- human naive B cells contain mostly autoreactive unresponsive clones.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
Macrophages from RA synovial fluids were compared to primary human blood-derived macrophages.
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
KLF7 null mice show profound axonal growth defects in the olfactory epithelium. The goal of this study was the identification of potential KLF7 target genes in olfactory sensory neurons.
Publication Title
Identification of genes regulated by transcription factor KLF7 in differentiating olfactory sensory neurons.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Most autoreactive B cells are normally counterselected during early B cell development. To determine whether Toll-like receptors (TLRs) regulate the removal of autoreactive B lymphocytes, we tested the reactivity of recombinant antibodies from single B cells isolated from patients deficient for IL-1R-associated kinase (IRAK)-4, myeloid differentiation factor 88 (MyD88) and UNC-93B. Indeed, all TLRs except TLR3 require IRAK-4 and MyD88 to signal and UNC-93B-deficient cells are unresponsive to TLR3, TLR7, TLR8 and TLR9. All patients suffered from defective central and peripheral B cell tolerance checkpoints resulting in the accumulation of large numbers of autoreactive mature nave B cells in their blood. Hence, TLR7, TLR8, and TLR9 may prevent the recruitment of developing autoreactive B cells in healthy donors. Paradoxically, IRAK-4-, MyD88- and UNC-93B-deficient patients did not display autoreactive antibodies in their serum nor developed autoimmune diseases, suggesting that IRAK-4, MyD88 and UNC-93B pathway blockade may thwart autoimmunity in humans.
Publication Title
IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans.
Sample Metadata Fields
No sample metadata fields
View Samples