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accession-icon GSE4600
Identifying targets of MeCP2 during neuronal maturational differentiation
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Rett syndrome (RTT) is an X-linked dominant neurodevelopmental disorder caused by mutations in MECP2, encoding methyl-CpG binding protein 2. MeCP2 is a transcriptional repressor elevated in mature neurons and is predicted to be required for neuronal maturation by regulating multiple target genes. Identifying primary gene targets in either Mecp2-deficient mice or human RTT brain has proven to be difficult, perhaps because of the transient requirement for MeCP2 during neuronal maturation. In order to experimentally control the timing of MeCP2 expression and deficiency during neuronal maturation, human SH-SY5Y cells undergoing mature neuronal differentiation were transfected with methylated MeCP2 oligonucleotide decoy to disrupt the binding of MeCP2 to endogenous targets. Genome-wide expression microarray analysis identified all four known members of the inhibitors of differentiation or inhibitors of DNA binding (ID1, ID2, ID3 and ID4) subfamily of helix-loop-helix (HLH) genes as novel neuronal targets of MeCP2. Chromatin immunoprecipitation analysis confirmed binding of MeCP2 near or within the promoters of ID1, ID2 and ID3, and quantitative RT-PCR confirmed increased expression of all four Id genes in Mecp2-deficient mouse brain. All four ID proteins were significantly increased in Mecp2-deficient mouse and human RTT brain using immunofluorescence and laser scanning cytometric analyses. Because of their involvement in cell differentiation and neural development, ID genes are ideal primary targets for MeCP2 regulation of neuronal maturation that may explain the molecular pathogenesis of RTT.

Publication Title

Inhibitors of differentiation (ID1, ID2, ID3 and ID4) genes are neuronal targets of MeCP2 that are elevated in Rett syndrome.

Alternate Accession IDs

E-GEOD-4600

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE46295
Effects of a Tricaprylin Emulsion on Anti-glomerular Basement Membrane Glomerulonephritis in Rats
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Expression data from rat with anti-glomerular basement membrane nephritis (anti-GBM). We used microarrays to analyze the transcriptome of kidney from anti-GBM model rat with or without drug treatment

Publication Title

Effects of a Tricaprylin Emulsion on Anti-glomerular Basement Membrane Glomerulonephritis in Rats: In Vivo and in Silico Studies.

Alternate Accession IDs

E-GEOD-46295

Sample Metadata Fields

Specimen part

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accession-icon GSE37173
elucidation a possible mechanism of kidney stone formation by using a MetS mouse model and to assess the effectiveness of adiponectin treatment in preventing kidney stones.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

we performed genome-wide expression analyses for investigating novel genetic environmental changes.

Publication Title

Effect of adiponectin on kidney crystal formation in metabolic syndrome model mice via inhibition of inflammation and apoptosis.

Alternate Accession IDs

E-GEOD-37173

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP107968
Integrative epigenomic analyses of early-life hypothalamic response to augmented maternal care [RNA-seq]
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The quality of maternal care in early-life plays a crucial role in mammalian neurodevelopment. Augmented maternal care (AMC) is a well-established rodent model of enhanced neonatal care. Rats that have undergone AMC have improved stress resilience and cognition compared with rats that have experienced normal levels of maternal care or adverse neonatal stress. However, the epigenomic basis of long-lived responses to AMC has not been previously explored. Thus, we employed whole-genome bisulfite sequencing (WGBS), RNA-sequencing (RNA-seq), and a multiplex microRNA (miRNA) assay to assess DNA cytosine methylation, gene expression, and miRNA expression, respectively. The integrated results identify a suite of 20 prioritized candidates impacted by AMC. Overall, these results identified AMC-induced regulatory differences in genes related to neurotransmission, neurodevelopment, protein synthesis, and oxidative phosphorylation in addition to the expected stress response genes. Together, these unbiased results represent a key progression in understanding the complex mechanisms underlying the early-life mechanisms for AMC programming stress resiliency. Overall design: DNA methylation and RNA were assayed in augmented maternal care male rats as well as controls.

Publication Title

Experience-dependent neuroplasticity of the developing hypothalamus: integrative epigenomic approaches.

Alternate Accession IDs

GSE99278

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject

View Samples
accession-icon GSE48029
Expression data of Jurkat cells stably expressing HBZ with or without stimulation
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human T-cell leukemia virus type 1 (HTLV-1) encodes HTLV-1 bZIP factor (HBZ), which is thought to be crucial for neoplastic and inflammatory diseases caused by HTLV-1. So, we analyzed the transcriptional profile of HBZ expressing cells and how HBZ affect the expression of apoptosis-related genes.

Publication Title

HTLV-1 bZIP factor suppresses apoptosis by attenuating the function of FoxO3a and altering its localization.

Alternate Accession IDs

E-GEOD-48029

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE57194
In Vitro Transformation of Primary Human CD34+ Cells by AML Fusion Oncogenes: Early Gene Expression Profiling Reveals Possible Drug Target in AML
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Different fusion oncogenes in acute myeloid leukemia (AML) have distinct clinical and laboratory features suggesting different modes of malignant transformation. Here we compare the in vitro effects of representatives of major groups of AML fusion oncogenes on primary human CD34+ cells.

Publication Title

In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML.

Alternate Accession IDs

E-GEOD-57194

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP096964
A de novo mouse model of C11orf95-RELA fusion-driven ependymoma identifies driver functions in addition to NF?B
  • organism-icon Mus musculus
  • sample-icon 38 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The vast majority of supratentorial ependymomas (ST-EPNs) have few mutations other than chromosomal rearrangements on chromosome 11, most generating a fusion between C11orf95 and RELA (CR). This CR fusion can transform stem cells ex vivo rendering them oncogenic and may possess NF-?B activity, which has been proposed to be a mechanism of oncogenesis. However, it is not known whether CR is sufficient for EPN formation in vivo, and from what cell type and location. We found that CR is sufficient to form tumors from cells in the ependymal zone in mice that show many molecular and histologic similarities to human ST-EPN. Furthermore, the activation of NF-?B by this fusion protein appears minimal and not related to its oncogenic activity Overall design: C11orf95-RELA is a potent oncogene for supratentorial ependymoma

Publication Title

A De Novo Mouse Model of C11orf95-RELA Fusion-Driven Ependymoma Identifies Driver Functions in Addition to NF-κB.

Alternate Accession IDs

GSE93765

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP067837
mRNA expression profile of Lymphocytes
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Va24 invariant natural killer T (iNKT) cells are a subset of T lymphocytes implicated in the regulation of broad immune responses. They recognize lipid antigens presented by CD1d on antigen-presenting cells and induce both innate and adaptive immune responses, which enhance effective immunity against cancer, represent promising therapeutic target. However, reduced iNKT-cell numbers and function have been observed in many patients with cancer. To overcome this obstacle, we reprogramed human iNKT cells to pluripotency and then redifferentiated into regenerated iNKT cells in vitro through IL-7/IL-15-based optimized cytokine combination. They showed proliferation and IFN-? production in response to a-galactosylceramide, induced dendritic cell maturation and downstream activation of cancer antigen-specific cytotoxic T lymphocytes in vitro, and exhibited NKG2D- and DNAM-1-mediated natural killer celllike cytotoxicity against cancer cell lines. Their immunological features and availability in an unlimited supply from induced pluripotent stem cells offer the potential to develop effective immunotherapies against cancer. Overall design: Expression profile of the lymphocytes (n = 17) by highthrouput sequencing

Publication Title

Cellular Adjuvant Properties, Direct Cytotoxicity of Re-differentiated Vα24 Invariant NKT-like Cells from Human Induced Pluripotent Stem Cells.

Alternate Accession IDs

GSE76371

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE102423
DNA microarray analysis of G9a knockout embryonic stem cells
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In embryonic stem cells (ESCs), the expression of development-related genes, including germ cellrelated genes, is globally repressed. The transcription factor MAX represses germ cellrelated gene expression in ESCs via PCGF6-polycomb repressive complex (PRC)1, which consists of several epigenetic factors. However, we predicted that MAX represses germ cellrelated gene expression through several additional mechanisms because PCGF6-PRC1 regulates the expression of only a subset of genes repressed by MAX. Here, we report that MAX associated with DNA methyltransferases (DNMTs) and the histone methyltransferase SETDB1 cooperatively control germ cellrelated gene expression in ESCs. Both DNA methylation and histone H3 lysine 9 tri-methylation of the promoter regions of several germ cellrelated genes were not affected by knockout of the PRC1 components, indicating that the MAX-DNMT and MAX-SETDB1 pathways are independent of the PCGF6-PRC1 pathway. Our findings provide insights into our understanding of MAX-based repressive mechanisms of germ cellrelated genes in ESCs.

Publication Title

DNMTs and SETDB1 function as co-repressors in MAX-mediated repression of germ cell-related genes in mouse embryonic stem cells.

Alternate Accession IDs

E-GEOD-102423

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE95278
Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Cutaneous exposure to food antigen through impaired skin barrier has been shown to induce epicutaneous sensitization, and thereby cause IgE-mediated food allergy.

Publication Title

Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice.

Alternate Accession IDs

E-GEOD-95278

Sample Metadata Fields

Sex, Specimen part

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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