Filters
Technology
Platform
GSE33516
Mus musculus
2 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We used microarray analysis to identify specific molecular mechanisms controlling IL-5 transcription in memory Th2 cells.
Publication Title
Eomesodermin controls interleukin-5 production in memory T helper 2 cells through inhibition of activity of the transcription factor GATA3.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Expression of genes related to fibrosis was assessed in the liver of AIM+/+ and AM-/- mice fed a high-fat diet (HFD) for various period. Overall, there was no significant difference in the magnitude of expression of fibrosis-related genes during the steatosis progression.
Publication Title
Circulating AIM prevents hepatocellular carcinoma through complement activation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Following antigen encounter by CD4 T cells, polarizing cytokines induce the expression of master regulators that control differentiation. Inactivation of the histone methyltransferase Ezh2 was found to specifically enhance T-helper (Th)1 and Th2 cell differentiation and plasticity. Ezh2 directly bound and facilitated correct expression of Tbx21 and Gata3 in differentiating Th1 and Th2 cells, accompanied by substantial tri-methylation at lysine 27 of histone 3 (H3K27-Me3). In addition, Ezh2 deficiency resulted in spontaneous generation of discrete IFN- and Th2 cytokine-producing populations in non-polarizing cultures, and under these conditions IFN- expression was largely dependent on enhanced expression of the transcription factor Eomesodermin. In vivo, Loss of Ezh2 caused increased pathology in a model of allergic asthma and resulted in progressive accumulation of memory phenotype Th2 cells. This study establishes a functional link between Ezh2 and transcriptional regulation of lineage-specifying genes in terminally differentiated CD4 T cells.
Publication Title
The polycomb protein Ezh2 regulates differentiation and plasticity of CD4(+) T helper type 1 and type 2 cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Memory helper T (Th) cells are crucial for secondary immune responses against infectious microorganisms but also drive the pathogenesis of chronic inflammatory diseases. Therefore, it is of fundamental importance to understand how memory T cells are generated. However, the molecular mechanisms governing memory Th cell generation remain incompletely understood. Here, we identified CD30 as a molecule heterogeneously expressed on effector Th1 and Th17 cells, and CD30hi effector Th1 and Th17 cells preferentially generated memory Th1 and Th17 cells. We found that CD30 mediated signal induced Transglutaminase-2 (TG2) expression, and that the TG2 expression in effector Th cells is essential for memory Th cell generation. In fact, Cd30-deficiency resulted in the impaired generation of memory Th1 and Th17 cells, which can be rescued by overexpression of TG2. Furthermore, transglutaminase-2 (Tgm2)-deficient CD4 T cells failed to become memory Th cells. As a result, T cells from Tgm2-deficient mice displayed impaired antigen-specific antibody production and attenuated Th17-mediated allergic responses. Our data indicate that CD30-induced TG2 expression in effector Th cells is essential for the generation of memory Th1 and Th17 cells, and that CD30 can be a marker for precursors of memory Th1 and Th17 cells.
Publication Title
Essential Role for CD30-Transglutaminase 2 Axis in Memory Th1 and Th17 Cell Generation.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 102 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Accumulating evidence suggests that mitochondrial dysfunction underlies the pathophysiology of bipolar disorder (BD) and schizophrenia (SZ). We performed large-scale DNA microarray analysis of postmortem brains of patients with BD or SZ, and examined expression patterns of mitochondria-related genes. We found a global down-regulation of mitochondrial genes, such as those encoding respiratory chain components, in BD and SZ samples, even after the effect of sample pH was controlled. However, this was likely due to the effects of medication. Medication-free patients with BD showed tendency of up-regulation of subset of mitochondrial genes. Our findings support the mitochondrial dysfunction hypothesis of BD and SZ pathologies. However, it may be the expression changes of a small fraction of mitochondrial genes rather than the global down-regulation of mitochondrial genes. Our findings warrant further study of the molecular mechanisms underlying mitochondrial dysfunction in BD and SZ.
Publication Title
Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis.
Sample Metadata Fields
No sample metadata fields
View Samples- Arabidopsis thaliana
- 4 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
AS1 and AS2 encode MYB related protein and AS2-domain containing protein, respectively and may regulate transcription. These genes are involved in the determination of axes of leaves of Arabidopsis thaliana. To know the gene regulation in the leaf development, expression profile among wild-type, as1 and as2 mutants and AS2 overexpression plants were compaired.
Publication Title
Meta-analyses of microarrays of Arabidopsis asymmetric leaves1 (as1), as2 and their modifying mutants reveal a critical role for the ETT pathway in stabilization of adaxial-abaxial patterning and cell division during leaf development.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 52 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
RHAU (RNA helicase-associated with AU-rich element) is a DExH protein that was originally identified as a factor accelerating AU-rich element-mediated mRNA degradation. The finding that RHAU is predominantly localized in the nucleus, despite that mRNA degradation occurs in cytoplasm, prompted us to consider nuclear functions of RHAU. In HeLa cells, RHAU was localized throughout the nucleoplasm with some concentration in nuclear speckles in a manner dependent on ATPase activity. Transcriptional arrest altered its localization to nucleolar caps where it was colocalized with other RNA helicases, p68 and p72, suggesting that RHAU is involved in transcription-related RNA metabolism in the nucleus. To see whether RHAU affects global gene expression either transcriptionally or posttranscriptionally, we performed microarray analysis using total RNA prepared from RHAU-depleted HeLa cell lines, measuring both steady-state mRNA levels and mRNA half-lives by ActinomycinD-chase. We found that most transcripts whose steady-state levels were affected by RHAU knockdown did not show changes in their half-lives, suggesting the involvement of transcriptional regulation for these transcripts. We propose that RHAU has dual functions involved in synthesis and degradation of mRNA in different subcellular compartments.
Publication Title
Transcription-dependent nucleolar cap localization and possible nuclear function of DExH RNA helicase RHAU.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 50 Downloadable Samples
- Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
We performed the oligonucleotide microarray analysis in bipolar disorder, major depression, schizophrenia, and control subjects using postmortem prefrontal cortices provided by the Stanley Foundation Brain Collection. By comparing the gene expression profiles of similar but distinctive mental disorders, we explored the uniqueness of bipolar disorder and its similarity to other mental disorders at the molecular level. Notably, most of the altered gene expressions in each disease were not shared by one another, suggesting the molecular distinctiveness of these mental disorders. We found a tendency of downregulation of the genes encoding receptor, channels or transporters, and upregulation of the genes encoding stress response proteins or molecular chaperons in bipolar disorder. Altered expressions in bipolar disorder shared by other mental disorders mainly consisted of upregulation of the genes encoding proteins for transcription or translation. The genes identified in this study would be useful for the understanding of the pathophysiology of bipolar disorder, as well as the common pathophysiological background in major mental disorders at the molecular level.
Publication Title
Molecular characterization of bipolar disorder by comparing gene expression profiles of postmortem brains of major mental disorders.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
Illumina HiSeq 2000
Description
We performed RNA-Seq on PHF21A-deficient patient-dervied lymphoblasts as well as two unaffected individuals. Overall design: We performed RNA-Seq from patient-derived lymphoblast cells. Libraries were polyA-selected and strand-specific according to the protocol described in PMID: 25607527
Publication Title
Transcriptome Analysis Revealed Impaired cAMP Responsiveness in PHF21A-Deficient Human Cells.
Sample Metadata Fields
Sex, Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The transcription factor c-MYC intron binding protein 1 (MIBP1) binds to various genomic regulatory regions, including intron 1 of c-MYC. This factor is highly expressed in post-mitotic neurons in the fetal brain and may be involved in various biological steps, such as neurological and immunological processes. In this study, we globally characterized the transcriptional targets of MIBP1 and proteins that interact with MIBP1. Microarray hybridization followed by Gene Set Enrichment Analysis revealed that genes involved in the pathways downstream of MYC, NF-B, and TGF- were downregulated when HEK293 cells stably overexpressed MIBP1. In silico transcription factor binding site analysis of the promoter regions of these downregulated genes showed that the NF-B binding site was the most overrepresented. The upregulation of genes known to be in the NF-B pathway after the knockdown of endogenous MIBP1 in HT1080 cells supports the view that MIBP1 is a downregulator of the NF-B pathway. We also confirmed the binding of the MIBP1 to the NF-B site. By immunoprecipitation and mass spectrometry, we detected O-linked -N-acetylglucosamine (O-GlcNAc) transferase (OGT) as a prominent binding partner of MIBP1. Analyses using deletion mutants revealed that a 154-amino acid region of MIBP1 was necessary for its OGT binding and O-GlcNAcylation. A luciferase reporter assay showed that NF-B-responsive expression was repressed by MIBP1, and stronger repression by MIBP1 lacking the 154-amino acid region was observed. Our results indicate that the primary effect of MIBP1 expression is the downregulation of the NF-B pathway, and that this effect is attenuated by O-GlcNAc signaling.
Publication Title
Genome-wide repression of NF-κB target genes by transcription factor MIBP1 and its modulation by O-linked β-N-acetylglucosamine (O-GlcNAc) transferase.
Sample Metadata Fields
Cell line
View Samples