This SuperSeries is composed of the SubSeries listed below.
Identification of genes with a correlation between copy number and expression in gastric cancer.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesTo elucidate gene expression associated with copy number changes, we performed a genome-wide copy number and expression microarray analysis of 25 pairs of gastric tissues.
Identification of genes with a correlation between copy number and expression in gastric cancer.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesDown syndrome (DS) is caused by triplication of Human chromosome 21 (Hsa21) and associated with an array of deleterious phenotypes, including mental retardation, heart defects and immunodeficiency. Genome-wide expression patterns of uncultured peripheral blood cells are useful to understanding of DS-associated immune dysfunction. We used a Human Exon microarray to characterize gene expression in uncultured peripheral blood cells derived from DS individuals and age-matched controls from two age groups: neonate (N) and child (C). A total of 174 transcript clusters (gene-level) with eight located on Hsa21 in N group and 383 transcript clusters including 56 on Hsa21 in C group were significantly dysregulated in DS individuals. Microarray data were validated by quantitative polymerase chain reaction. Functional analysis revealed that the dysregulated genes in DS were significantly enriched in two and six KEGG pathways in N and C group, respectively. These pathways included leukocyte trans-endothelial migration, B cell receptor signaling pathway and primary immunodeficiency, etc., which causally implicated dysfunctional immunity in DS. Our results provided a comprehensive picture of gene expression patterns in DS at the two developmental stages and pointed towards candidate genes and molecular pathways potentially associated with the immune dysfunction in DS.
Genome-wide expression analysis in Down syndrome: insight into immunodeficiency.
Sex, Age, Specimen part, Disease
View SamplesSox31 is a member of the zebrafish SoxB1 subfamily, and its expression can be detected both pre- and post-MBT. To distinguish the function of its maternal and zygotic transcripts, a splice blocking morpholino (Sb MO) was designed to interfere with the processing of new, zygotically synthesised mRNAs without interfering with mRNAs of maternal origin. Developmental arrest was observed in Sb MO which could not bypass MBT.
Splice blocking of zygotic sox31 leads to developmental arrest shortly after Mid-Blastula Transition and induces apoptosis in zebrafish.
No sample metadata fields
View SamplesCHD3 proteins are ATP-dependent chromatin remodeling factors that are components of diverse multisubunit complexes that can either repress or activate gene expression. In plants, the CHD3 protein PICKLE (PKL) is necessary for repression of seed-specific genes during germination and promotes deposition of the repressive epigenetic mark trimethylation of histone H3 lysine 27 (H3K27me3). It is unknown, however, if PKL acts directly at H3K27me3-enriched loci. We undertook a microarray analysis of 14-day-old plants and found that PKL continues to play an important role in expression of H3K27me3-enriched genes and in specification of developmental identity after germination.
No associated publication
Specimen part
View SamplesGAS2DN could suppress the growth of chronic myeloid leukemia cells, including K562, MEG-01 and CD34+ cells from patients. In addition, GAS2DN inhibited the tumorigenic ability of MEG-01 cells in nude mice. To understand the molecular insight of this inhibitory effect of GAS2DN, global gene expression were performed.
No associated publication
Cell line
View SamplesIdentify the PDX model of DLBCL subtypes by the microarray expression profiling
No associated publication
Specimen part, Subject
View SamplesRegulatory T cells (Treg) are pivotal for the maintenance of peripheral tolerance by controlling self-reactive, chronic and homeostatic T cell responses. We now report that the increase in Treg suppressive function observed in lymphopenic mice correlates with the degree of lymphopenia and is caused by a higher frequency of a novel subpopulation of CD103posICOSpos cells among peripheral Treg that differentially express multiple Treg signature genes.
A subpopulation of CD103(pos) ICOS(pos) Treg cells occurs at high frequency in lymphopenic mice and represents a lymph node specific differentiation stage.
Sex, Age, Specimen part
View SamplesMultipotent progenitors (MPP) and common dendritic cell progenitors (CDP) were obtained from mouse bone marrow, followed by in vitro culture with a specific cytokine cocktail and FACS sorting (Felker et al., 2010; Ser et al., 2012). Cells were treated with 10 ng/ml recombinant human TGF-1 (R&D Systems, Minneapolis, USA) for 2, 4, 8, 12 and 24 h as described (Felker et al., 2010) or left untreated.
TGF-β stimulation in human and murine cells reveals commonly affected biological processes and pathways at transcription level.
Specimen part
View SamplesEed (embryonic ectoderm development) is a core component of the Polycomb Repressive Complex 2 (PRC2) which catalyzes the methylation of histone H3 lysine 27 (H3K27). Trimethylated H3K27 (H3K27me3) can act as a signal for PRC1 recruitment in the process of gene silencing and chromatin condensation. Previous studies with Eed KO ESCs revealed a failure to down-regulate a limited list of pluripotency factors in differentiating ESCs. Our aim was to analyze the consequences of Eed KO for ESC differentiation. To this end we first analyzed ESC differentiation in the absence of Eed and employed in silico data to assess pluripotency gene expression and H3K27me3 patterns. We linked these data to expression analyses of wildtype and Eed KO ESCs. We observed that in wildtype ESCs a subset of pluripotency genes including Oct4, Nanog, Sox2 and Oct4 target genes progressively gain H3K27me3 during differentiation. These genes remain expressed in differentiating Eed KO ESCs. This suggests that the deregulation of a limited set of pluripotency factors impedes ESC differentiation. Global analyses of H3K27me3 and Oct4 ChIP-seq data indicate that in ESCs the binding of Oct4 to promoter regions is not a general predictor for PRC2-mediated silencing during differentiation. However, motif analyses suggest a binding of Oct4 together with Sox2 and Nanog at promoters of genes that are PRC2-dependently silenced during differentiation. In summary, our data further characterize Eed function in ESCs by showing that Eed/PRC2 is essential for the onset of ESC differentiation.
Polycomb protein EED is required for silencing of pluripotency genes upon ESC differentiation.
Specimen part, Cell line
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