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GSE104175
Homo sapiens
2 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
It has been difficult to elucidate the structure of gene regulatory networks under anticancer drug treatment. Here, we developed an algorithm to highlight the hub genes that play a major role in creating the upstream and downstream relationships within a given set of differentially expressed genes. The directionality of the relationships between genes was defined using information from comprehensive collections of transcriptome profiles after gene knockdown and overexpression. As expected, among the drug-perturbed genes, our algorithm tended to derive plausible hub genes, such as transcription factors. Our validation experiments successfully showed the anticipated activity of certain hub gene in establishing the gene regulatory network that was associated with cell growth inhibition. Notably, giving such top priority to the hub gene was not achieved by ranking fold change in expression and by the conventional gene set enrichment analysis of drug-induced transcriptome data. Thus, our data-driven approach can facilitate to understand drug-induced gene regulatory networks for finding potential functional genes.
Publication Title
InDePTH: detection of hub genes for developing gene expression networks under anticancer drug treatment.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Genome U95A Array (hgu95a)
Description
Gene expression profiling was performed on biopsies of affected and unaffected psoriatic skin and normal skin from seven Japanese patients to obtain insights into the pathways that control this disease. U95A Affymetrix DNA chips that contain oligonucleotide arrays of approximately 12,000 well-characterized human genes were used in the study. The statistical analysis of the Affymetrix data, based on the ranking of the Student-test statistic, revealed a complex regulation of molecular stress and immune gene responses. The majority of the 266 induced-genes in affected and unaffected psoriatic skin were involved with interferon mediation, immunity, cell-adhesion, cytoskeleton restructuring, protein trafficking and degradation, RNA regulation and degradation, signaling transduction, apoptosis and atypical epidermal cellular proliferation and differentiation. The disturbances in the normal protein degradation equilibrium of skin were reflected by the significant increase in the gene expression of various protease inhibitors and proteinases including the induced components of the ATP/ubiquitin-dependent non-lysosomal proteolytic pathway that is involved with peptide processing and presentation to T-cells. Some of the upregulated genes, such as TGM1, IVL, CSTA, FABP5 and SPRR, are well known psoriatic markers involved in atypical epidermal cellular organization and differentiation. In the comparison between the affected and unaffected psoriatic skin, the transcription factor JUNB was found at the top of the statistical rankings for the 51 significantly upregulated genes in affected skin, suggesting that it has an important but as yet undefined role in psoriasis. Our gene expression data and analysis suggest that psoriasis is a chronic IFN and T-cell-mediated immune disease of the skin where the imbalance in epidermal cellular structure, growth and differentiation arises from the molecular antiviral stress signals initiating inappropriate immune responses.
Publication Title
Gene expression profiling of Japanese psoriatic skin reveals an increased activity in molecular stress and immune response signals.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 19 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The ERK family of MAP kinase plays a critical role in growth factor-stimulated cell cycle progression from G0/G1 to S phase. But, how sustained activation of ERK promotes G1 progression has remained unclear. Here, our systematic analysis on the temporal program of ERK-dependent gene expression shows that sustained activation of ERK is required for induction and maintenance of the decreased expression levels of a set of genes. Moreover, our cell biological analysis reveals that these ERK-dependent downregulated genes have the ability to block S phase entry. Cessation of ERK activation at mid or late G1 leads to a rapid increase of these anti-proliferative genes and results in the inhibition of S phase entry. These findings uncover an important mechanism by which the duration of ERK activation regulates cell cycle progression through dynamic changes in gene expression, and identify novel ERK target genes crucial for the regulation of cell cycle progression.
Publication Title
Continuous ERK activation downregulates antiproliferative genes throughout G1 phase to allow cell-cycle progression.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
Ion Torrent Proton
Description
We explored the mechanism by which TLP affects DNA damage response. We performed mRNA-seq analysis of non-treated and etoposide-treated samples in control and TLP-knockdown cells. We show that TLP is critical for global transcriptional repression after double-strand DNA breaks (DSBs). Overall design: Examination of non-treated and etoposide-treated samples in control and TLP-knockdown cells
Publication Title
TLP-mediated global transcriptional repression after double-strand DNA breaks slows down DNA repair and induces apoptosis.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs.
Publication Title
CUGBP1 and MBNL1 preferentially bind to 3' UTRs and facilitate mRNA decay.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 4 Downloadable Samples
- Ion Torrent Proton
Description
The goal of this study was to elucidate the effects of inflammation on bone metabolism. As we found IL-17A is induced immediately after bone injury and Il17a-/- mice showed delayed healing, we analyzed the effects of IL-17A on mesenchymal cells in the repair tissue. Most of the IL-17RA+ cells were PaS cells. We collected these cells and analyzed their response to IL-17A by RNA sequencing. This analysis will provide a mechanistic insight into the mechanism of how IL-17A promote bone formation in the context of bone fracture healing. Overall design: PaS cells were harvested from the injury tissue of wild-type mice and cultured with or without IL-17A or BMP-2. RNAs were harvested at day 7.
Publication Title
IL-17-producing γδ T cells enhance bone regeneration.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 1500
Description
Memory helper T cells provide long-lasting host defeMemory helper T cells provide long-lasting host defense against microbial pathogens, while distinct subpopulations of memory T cells drive chronic inflammatory diseases such as asthma. Asthma is a chronic allergic inflammatory disease with airway remodeling including fibrotic changes. The immunological mechanisms that induce airway fibrotic changes in allergic inflammation remain unknown. We found that Interleukin-33 (IL-33) enhanced Amphiregulin production by the IL-33 receptor, ST2hi memory T helper-2 (Th2) cells. Amphiregulin-epidermal growth factor receptor (EGFR)-mediated signaling directly reprogramed eosinophils to an inflammatory state with enhanced production of Osteopontin, a key profibrotic immunomodulatory protein. IL-5-producing memory Th2 cells and Amphiregulin-producing memory Th2 cells appeared to cooperate to establish lung fibrosis. The analysis of polyps from patients with eosinophilic chronic rhinosinusitis revealed fibrosis with accumulation of Amphiregulin-producing CRTH2hiCD161hiCD45RO+CD4+ Th2 cells and Osteopontin-producing eosinophils. Thus, the IL-33-Amphiregulin-Osteopontin axis directs fibrotic responses in eosinophilic airway inflammation and is a potential target for the treatment of fibrosis induced by chronic allergic disorders. against microbial pathogens, while distinct subpopulations of memory T cells drive chronic inflammatory diseases such as asthma. Asthma is a chronic allergic inflammatory disease with airway remodeling including fibrotic changes. The immunological mechanisms that induce airway fibrotic changes in allergic inflammation remain unknown. We found that Interleukin-33 (IL-33) enhanced Amphiregulin production by the IL-33 receptor, ST2Â hi memory T helper-2 (Th2) cells. Amphiregulin-epidermal growth factor receptor (EGFR)-mediated signaling directly reprogramed eosinophils to an inflammatory state with enhanced production of Osteopontin, a key profibrotic immunomodulatory protein. IL-5-producing memory Th2 cells and Amphiregulin-producing memory Th2 cells appeared to cooperate to establish lung fibrosis. The analysis of polyps from patients with eosinophilic chronic rhinosinusitis revealed fibrosis with accumulation of Amphiregulin-producing CRTH2hiCD161hiCD45RO+CD4+ Th2 cells and Osteopontin-producing eosinophils. Thus, the IL-33-Amphiregulin-Osteopontin axis directs fibrotic responses in eosinophilic airway inflammation and is a potential target for the treatment of fibrosis induced by chronic allergic disorders. Overall design: Amphiregulin producing cells, eosinophils and lung treated with HDM are assessed by RNA-seq.
Publication Title
Amphiregulin-Producing Pathogenic Memory T Helper 2 Cells Instruct Eosinophils to Secrete Osteopontin and Facilitate Airway Fibrosis.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 68 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
During cerebral development, a variety of neurons are sequentially generated by self-renewing progenitor cells, apical progenitors (APs). A temporal change in AP identity is thought to produce a diversity of progeny neurons, while underlying mechanisms are largely unknown. Here we performed single cell genome-wide transcriptome profiling of APs at different neurogenic stages, and identified a set of genes that are temporally expressed in APs in a manner independent of differentiation state. Surprisingly, the temporal pattern of such AP gene expression was not affected by arresting cell cycling. Consistently, a transient cell cycle arrest of APs in vivo did not prevent descendant neurons to acquire their correct laminar fates. in vitro cell culture of APs revealed that transitions in AP gene expression involved in both cell-autonomous and non-autonomous mechanisms. These results suggest that timers controlling AP temporal identity run independently of cell cycle progression and Notch activation mode.
Publication Title
Cell-cycle-independent transitions in temporal identity of mammalian neural progenitor cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 39 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We generated hiPSCs from patients fibloblast with retinitis pigmentosa (RP) using retrovirus and Sendai virus vectors, which we differentiated into hiPSC derived retinal pigment epithelium using two different methods (SDIA and SFEB methods).
Publication Title
Characterization of human induced pluripotent stem cell-derived retinal pigment epithelium cell sheets aiming for clinical application.
Sample Metadata Fields
Cell line
View Samples- Arabidopsis thaliana
- 8 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Arabidopsis ABA hpersensitive germination2-1 mutant shows an enhanced sensitivity to ABA. This mutant has higher levels of endogenous ABA. This mutant also exhibited SA hypersensitivity and dwarf phenotype. Regarding SA hypersensitivity, ahg2-1 exhibits higher endogenous SA level and an enhanced resistance to pathogenic bacteria. Since AHG2 encodes the Arabidopsis polyA specific ribonuclease that is involved in mRNA degradation, presumably abnormal accumulation of some mRNAs confers the unique phenotype. Transcriptome analyses are expected to offer information on the target of AHG2. In order to eliminate secondary effects of higher levels of ABA and SA, ahg2-1abi1-1 and ahg2-1sid2-2 double mutants were also examined. The transcriptome data revealed that; ahg2-1 confers unique gene expression profiles, ABA and SA affect the expression profiles of this mutant but many genes are independent of those plant hormone responses. Comparing with expression profiles of other mutants indicated that the ahg2-1 might affect mitochondrial function.
Publication Title
ABA hypersensitive germination2-1 causes the activation of both abscisic acid and salicylic acid responses in Arabidopsis.
Sample Metadata Fields
No sample metadata fields
View Samples