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GSE9316
Mus musculus
12 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Th17 cells are enriched by sorting FR4-CD4+ T cells from SKG mice. A large number of Th17 cells also develop spontaneously when CD4+ T cells from IFN-g-deficient (IFN-g-/-) BALB/c mice are transferred to T cell-deficient RAG2-deficient (RAG2-/-) mice and subjected to homeostatic proliferation, whereas they fail to develop in similar transfer of IL-6-deficient (IL-6-/-) CD4+ T cells to IL-6-/- RAG2-/- mice.
Publication Title
Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We found a new spontaneous mutant mouse, laggard, characterized by general weakness in movements and retardation in growth.
Publication Title
Kif14 mutation causes severe brain malformation and hypomyelination.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
Analysis to find splicing variants that are differentially expressed in a highly metastatic stomach cancer cell line, MKN45P, versus its parental cell line, MKN45
Publication Title
Identification of a novel protein isoform derived from cancer-related splicing variants using combined analysis of transcriptome and proteome.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Rattus norvegicus
- 30 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
Microglia are key regulators of inflammatory response after stroke and brain injury. Here we profiled the microglia transcriptome isolated from a spontaneously hypertensive rat model of focal cerebral ischemia.
Publication Title
Transcriptomic characterization of microglia activation in a rat model of ischemic stroke.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 4 Downloadable Samples
IlluminaHiSeq2000, IlluminaGenomeAnalyzerIIx
Description
In the advanced stages of cancer, autophagy is thought to promote tumor progression through its ability to mitigate various cellular stresses. However, the details of how autophagy is homeostatically regulated in such tumors are unknown. Here, we report that NUPR1 (nuclear protein 1, transcriptional regulator), a transcriptional coregulator, is aberrantly expressed in a subset of cancer cells and predicts low overall survival rates for lung cancer patients. NUPR1 regulates the late stages of autolysosome processing through the induction of the SNARE protein SNAP25, which forms a complex with the lysosomal SNARE associated protein VAMP8. NUPR1 depletion deregulates autophagic flux and impairs autolysosomal clearance, inducing massive cytoplasmic vacuolization and premature senescence in vitro and tumor suppression in vivo. Collectively, our data show that NUPR1 is a potent regulator of autolysosomal dynamics and is required for the progression of some epithelial cancers. Overall design: mRNA profiles of NUPR1-depleted A549 and control cells were generated by RNA-sequencing, using Illumina GAIIx or Illumina HiSeq 2000.
Publication Title
NUPR1 maintains autolysosomal efflux by activating SNAP25 transcription in cancer cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
More effective therapeutic approaches for castration-resistant prostate cancer (CRPC) are urgently needed, thus reinforcing the need to understand how prostate tumors progress to castration resistance. We have established a novel mouse xenograft model of prostate cancer, KUCaP-2, which expresses the wild-type androgen receptor (AR) and which produces the prostate-specific antigen (PSA). In this model, tumors regress soon after castration, but then reproducibly restore their ability to proliferate after 1 to 2 months without AR mutation, mimicking the clinical behavior of CRPC. In the present study, we used this model to identify novel therapeutic targets for CRPC. Evaluating tumor tissues at various stages by gene expression profiling, we discovered that the prostaglandin E receptor EP4 subtype (EP4) was significantly upregulated during progression to castration resistance. Immunohistochemical results of human prostate cancer tissues confirmed that EP4 expression was higher in CRPC compared with hormone-nave prostate cancer. Ectopic overexpression of EP4 in LNCaP cells (LNCaP-EP4 cells) drove proliferation and PSA production in the absence of androgen supplementation in vitro and in vivo. Androgen-independent proliferation of LNCaP-EP4 cells was suppressed when AR expression was attenuated by RNA interference. Treatment of LNCaP-EP4 cells with a specific EP4 antagonist, ONO-AE3-208, decreased intracellular cyclic AMP levels, suppressed PSA production in vitro, and inhibited castration-resistant growth of LNCaP-EP4 or KUCaP-2 tumors in vivo. Our findings reveal that EP4 overexpression, via AR activation, supports an important mechanism for castration-resistant progression of prostate cancer. Furthermore, they prompt further evaluation of EP4 antagonists as a novel therapeutic modality to treat CRPC.
Publication Title
Identification of EP4 as a potential target for the treatment of castration-resistant prostate cancer using a novel xenograft model.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
WFS1 gene is coding protein with unknown function but its functional deficiency causes different neuropsychiatric and neuroendocrine syndromes. In the present study we aimed to find the functional networks influenced by the Wfs1 deficiency in the hypothalamus. We performed gene expression profiling (Mouse Gene 1.0 ST Arrays) in Wfs1 deficient mice (ko). Modified t-statistics was used for comparison of groups (wt vs ko). Functional annotation of the alterations in RNA levels was performed with Ingenuity Pathway Analysis. 305 genes were differentially expressed with nominal p-value less than 0.01. FDR adjusted p-values were significant (0.007) only for two genes C4b (t=9.66) and Wfs1 (t=-9.03). However, several genes related to the G-protein signalling were very close to the FDR adjusted significance. For instance, Rgs4 (regulator of G-protein signalling 4) was down-regulated (-0.34, t=-5.4) in Wfs1 deficient mice. Changes in Rgs4 and C4B expression were confirmed by QRT-PCR. In humans, Rgs4 is in the locus for bipolar disease (BPD) and its expression is down-regulated in BPD. C4b is the gene related to the neurodegenerative diseases. In conclusion, hypothalamic gene expression profiling indicates alterations in some functionally relevant molecular pathways explaining the clinical syndrome in the Wolfram syndrome patients.
Publication Title
Hypothalamic gene expression profile indicates a reduction in G protein signaling in the Wfs1 mutant mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Background: It is recognized that atherosclerosis can regresses at least in animal models. However, little is known about the mechanisms. We induced regression of advanced atherosclerosis in apolipoprotein E deficient (APOE/) mice and studied underlying mechanisms. Unexpectedly, our study led to the role of interleukin-7 (IL-7) in atherogenesis.
Publication Title
Interleukin-7 induces recruitment of monocytes/macrophages to endothelium.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
MicroRNAs are small non-coding RNA species, some of which are playing important roles in cell differentiation. However, the level of participations of microRNAs in epithelial cell differentiation is largely unknown. Here, we found that expression levels of four microRNAs (miR-210, miR-338-3p, miR-33a and miR-451) were significantly increased in differentiated stage of T84 cells, compared with undifferentiated stage. Additionally, we demonstrate that miR-338-3p and miR-451 contribute to the formation of epithelial basolateral polarity by facilitating translocalization of beta1 integrin to the basolateral membrane. However, candidate target mRNAs of miR-338-3p and miR-451 and the mechanism behind observed phenomena is uncertain. Then, we performed comprehensive gene expression analysis to identify candidate target mRNAs and understand their mechanisms.
Publication Title
MicroRNA-338-3p and microRNA-451 contribute to the formation of basolateral polarity in epithelial cells.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Mus musculus
- 4 Downloadable Samples
- Ion Torrent Proton
Description
Protein arginine methylation is a post-translational modification catalyzed by protein arginine methyltransferase (PRMT). To elucidate the role of PRMT5 in T cells, we generated T-cell specific PRMT5-deficient mice (Prmt5 flox/d Cd4-Cre mice) and found a severe loss of thymic iNKT cells as well as a reduced number in peripheral CD4+ and CD8+ T cells. As iNKT cells were significantly decreased in the stage 1, 2 and 3 of developmental stages, RNA-seq was performed using stage 1 iNKT cells of control and PRMT5-deficient mice. This transcriptome analysis will provide mechanistic insight into how PRMT5 contributes to thymic iNKT cell development. Overall design: Stage 1 iNKT cells were sorted from thymus of control and Prmt5 flox/D Cd4-Cre mice. Total RNA was extracted and RNA-seq was performed by Ion Proton.
Publication Title
Arginine methylation controls the strength of γc-family cytokine signaling in T cell maintenance.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples