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GSE45558
Homo sapiens
45 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Melanoma cell lines were assessed for differences in gene expression patterns between the lines sensitive and resistant to BRAF and MEK inhibitor drugs.
Publication Title
The transcription cofactor c-JUN mediates phenotype switching and BRAF inhibitor resistance in melanoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus, Rattus norvegicus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Dual-mode modulation of Smad signaling by Smad-interacting protein Sip1 is required for myelination in the central nervous system.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and -catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair.
Publication Title
Dual-mode modulation of Smad signaling by Smad-interacting protein Sip1 is required for myelination in the central nervous system.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 13 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Association of juvenile spondyloarthritis (jSpA) with the HLA-B27 genotype is well established, but there is little knowledge of other genetic factors with a role in disease development. The aim of the present study was to identify and confirm gene signatures and novel biomarkers in various cohorts of untreated and treated patients diagnosed with jSpA and other forms of juvenile idiopathic arthritis (JIA).
Publication Title
Aberrant expression of shared master-key genes contributes to the immunopathogenesis in patients with juvenile spondyloarthritis.
Sample Metadata Fields
Sex, Specimen part, Disease
View Samples- Homo sapiens
- 12 Downloadable Samples
Illumina HiSeq 2500
Description
We used high throughput sequencing to analyze the transcriptional profiling of EVT. By comparing the transcriptional profiling of EVT with or without H19 knockdown, numerous genes showed significantly altered expression as a result of H19 repression. Overall design: HTR cells were transfected with either control siRNA or siH19. 48h later after transfection, total RNA was extracted for library preparation and RNA-seq analysis to compare trancript profiles between siCon and siH19 cells.
Publication Title
H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction.
Sample Metadata Fields
Cell line, Subject, Time
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
A predictive gene list for response to high dose melphalan therapy in patients diagnosed with multiple myeloma is generated by combining results from dose response experiments and microarray data using a B-cell line panel and the introduction of multivariate regression techniques.
Publication Title
Generation of a predictive melphalan resistance index by drug screen of B-cell cancer cell lines.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 38 Downloadable Samples
- Illumina HumanRef-8 v3.0 expression beadchip
Description
Gene expression analyis of two neonatal fibroblasts (BJ and HFF1), one adult dermal fibroblasts (NFH2), two BJ-derived human iPSCs (iB4 and iB5), two HFF1-derived iPSCs (iPS 2 and iPS4), four NFH2-derived iPSCs (OiPS3, OiPS6, OiPS8, OiPS16), one amniotic fluid cells and three derived iPSCs (lines 4, 5, 6, 10, and 41), two human ES cells (H1 and H9), neonatal fibroblasts transduced with the four retroviral factors (OKSM) after 24h, 48h, and 72h, neonatal fibroblasts treated with EDHB for 24h, 48h, and 72h, neonatal fibroblasts transduced with four factors and treated with EDHB for 24h, 48h, and 72h, neonatal fibroblasts knocked down for HIF1A (HIF1-KD) and for a scrambled sequence (SCR-KD)
Publication Title
HIF1α modulates cell fate reprogramming through early glycolytic shift and upregulation of PDK1-3 and PKM2.
Sample Metadata Fields
Age, Specimen part, Cell line
View Samples- Escherichia coli
- 8 Downloadable Samples
- Illumina Genome Analyzer II
Description
As nascent polypeptides exit ribosomes, they are engaged by a series of processing, targeting and folding factors. Here we present a selective ribosome profiling strategy that enables global monitoring of when these factors engage polypeptides in the complex cellular environment. Studies of the Escherichia coli chaperone Trigger Factor (TF) reveal that, while TF can interact with many polypeptides, ß-barrel outer membrane proteins are the most prominent substrates. Loss of TF leads to broad outer membrane defects and premature, cotranslational protein translocation. While in vitro studies suggested that TF is prebound to ribosomes waiting for polypeptides to emerge from the exit channel, we find that in vivo TF engages ribosomes only after ~100 amino acids are translated. Moreover, excess TF interferes with cotranslational removal of the N-terminal formyl methionine. Our studies support a triaging model in which proper protein biogenesis relies on the fine-tuned, sequential engagement of processing, targeting ad folding factors. Overall design: Examination of translation in the Gram-negative bacterium Escherichia coli, as well as an analysis of the interactions between nascent chains and the molecular chaperone Trigger Factor.
Publication Title
Selective ribosome profiling reveals the cotranslational chaperone action of trigger factor in vivo.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 1 Downloadable Sample
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
MicroRNAs predominantly decrease gene expression; however, specific mRNAs are translationally upregulated in quiescent (G0) mammalian cells and immature Xenopus laevis oocytes by an FXR1a-associated microRNP (microRNA-protein complex) that lacks the microRNP repressor, GW182. We conducted global proteomic analysis in THP1 cells depleted of FXR1 to globally identify activation targets of more than one microRNA, since FXR1 is required for microRNAmediated translation activation in THP1 G0 cells by FXR1-microRNPs.Since proteomic data changes could also be due to changes at the RNA level, total RNA levels in FXR1knockdown compared to control shRNA cells were examined in parallel by microarray analysis using Affymetrix Human GeneChip 2.0 ST.
Publication Title
A Specialized Mechanism of Translation Mediated by FXR1a-Associated MicroRNP in Cellular Quiescence.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Diet-induced obesity is reported to induce a phenotypic switch in adipose tissue macrophages from an antiinflammatory M2 state to a proinflammatory M1 state. Telmisartan, an angiotensin II type 1 receptor antagonist and a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist, reportedly has beneficial effects on insulin sensitivity. We studied the effects of telmisartan on the adipose tissue macrophage phenotype in high fat-fed mice. Telmisartan was administered for 5 weeks to high fat-fed C57BL/6 mice. Insulin sensitivity, macrophage infiltration, and the gene expressions of M1 and M2 markers in epididymal fat tissues were examined. Insulin- or a glucose-tolerance test showed that telmisartan treatment improved insulin resistance, decreasing the body weight gain, visceral fat weight and adipocyte size without affecting the amount of food intake. Telmisartan treatment reduced the number of CD11c-positive cells and crown-like structures. Telmisartan reduced the mRNA expressions of M1 macrophage markers, such as TNF-alpha and IL-6, and increased the expression of M2 markers, such as IL-10 and Mgl2. The reduction of M1 macrophage markers, as well as the increased gene expression of M2 markers especially IL-10, is a possible mechanism for the improvement of insulin sensitivity by telmisartan.
Publication Title
Telmisartan improves insulin resistance and modulates adipose tissue macrophage polarization in high-fat-fed mice.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples