Filters
Technology
Platform
GSE32984
Homo sapiens
14 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The endothelial transcription factor Erg (Ets Related Gene) plays an important role in homeostasis and angiogenesis by regulating many endothelial functions including survival and junction stability. Here we show that Erg regulates endothelial cell migration. Transcriptome profiling of Erg-deficient endothelial cells (EC) identified 80 genes involved in cell migration as candidate Erg targets, including regulators of the Rho GTPases. Inhibition of Erg expression in human umbilical vein endothelial cells (HUVEC) resulted in decreased migration in vitro, whilst Erg over-expression using adenovirus caused increased migration. Live-cell imaging of Erg-deficient HUVEC showed a reduction in lamellipodia, in line with decreased motility. Both actin and tubulin cytoskeletons were disrupted in Erg-deficient EC, with a dramatic increase in tubulin acetylation. Amongst the most significant microarray hit was the cytosolic histone deacetylase (HDAC)-6, a regulator of cell migration. Rescue experiments confirmed that HDAC6 mediates the Erg-dependent regulation of tubulin acetylation and actin localization.
Publication Title
The transcription factor Erg regulates expression of histone deacetylase 6 and multiple pathways involved in endothelial cell migration and angiogenesis.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Analysis of gene expression profiles in Induced T-to-Natural Killer (ITNK), compared to DN3 parental T cells and IL-2-expanded NK cells (LAK). The hypothesis tested in the present study was that gene expression profiles of ITNK that were derived from DN3 T cells after deletion of Bcl11b were more similar to LAK, rather than DN3 T cells. Results provide important information of the ITNKs, such as canditate genes regulated by Bcl11b, up-regulated important genes expressed in NK cells, and down-regulated T cell genes.
Publication Title
Reprogramming of T cells to natural killer-like cells upon Bcl11b deletion.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 19 Downloadable Samples
Illumina HiSeq 2000, Illumina HiSeq 2500
Description
We assessed global gene expression profiles in two mouse models of oncogenic FLT3-driven leukemia in the presence and absence of Dnmt3a. Overall design: Mouse mRNA profiles of Dnmt3aKO/FLT3-ITD leukemias, FLT3-ITD leukemias, normal CD4+/CD8+ thymocytes, Dnmt3aKO thymocytes, heterozygous Dnmt3a/heterozygous Flt3-ITD knockin leukemia, and heterozygous Flt3-ITD knockin pre-leukemic bone marrow cells were obtained by sequencing on Illumina HiSeq 2000 or 2500.
Publication Title
DNMT3A Loss Drives Enhancer Hypomethylation in FLT3-ITD-Associated Leukemias.
Sample Metadata Fields
No sample metadata fields
View Samples- Escherichia coli k-12
- 7 Downloadable Samples
- Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
MgrR is a newly characterized Hfq dependent small RNA RNA. The expression of MgrR is regulated by Two component system, PhoPQ regulon, which senses low Mg2+ in environment. It has been reported that Hfq-binding sRNAs base pair with target RNAs, frequently leading to rapid degradation of target messages or, less frequently, to stabilization, both of which can be assayed by using microarrays. In order to search for the target genes of MgrR, we therefore examined the consequences of MgrR expression on mRNA abundance under two conditions. In condition 1, the chromosomal copy of mgrR was deleted and MgrR was expressed for 15 from an induced plac-mgrR plasmid and compared to cells carrying a vector induced for the same period. In condition 2, the expression of mRNAs was compared in wild-type cells (mgrR+) and the mgrR deletion strain, both grown in LB; because MgrR levels are fairly high under our normal growth conditions, this allowed analysis of both the direct and indirect (long-term) effects of MgrR.
Publication Title
A PhoQ/P-regulated small RNA regulates sensitivity of Escherichia coli to antimicrobial peptides.
Sample Metadata Fields
No sample metadata fields
View Samples- Escherichia coli
- 20 Downloadable Samples
- Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
Transcription termination factor Rho is essential in enterobacteria. We inhibited Rho activity with bicyclomycin and used microarray experiments to assess Rho function on a genome-wide scale. Rho is a global regulator of gene expression that matches E. coli transcription to translational needs. Remarkably, genes that are most repressed by Rho are prophages and other horizontally-acquired portions of the genome. Elimination of these foreign DNA elements increases resistance to bicyclomycin. Although rho remains essential, such reduced-genome bacteria no longer require Rho cofactors NusA and NusG. Thus, Rho termination, supported by NusA and NusG, is required to suppress the toxic activity of foreign DNA.
Publication Title
Termination factor Rho and its cofactors NusA and NusG silence foreign DNA in E. coli.
Sample Metadata Fields
Compound
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
To determine whether the polyamide-Chl conjugate 1R-Chl would cause similar changes in global gene expression in K562 cells, affymetrix gene chip analysis was performed using 1R-Chl. Through class comparison analysis, 1R-Chl affected the levels of transcription and genes of interest were determined.
Publication Title
Small molecules targeting histone H4 as potential therapeutics for chronic myelogenous leukemia.
Sample Metadata Fields
Sex, Age, Disease
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Lymphoblast cells from a patient with Freidriech's Ataxia were incubated with pyrrole-imidazole polyamides targeted to the GAA triplet repeat in the intron 1. The polyamides were shown in cell culture to increase levels of endogenous frataxin mRNA. A normal sibling derived lymphoblast cell line was used as a control.
Publication Title
DNA sequence-specific polyamides alleviate transcription inhibition associated with long GAA.TTC repeats in Friedreich's ataxia.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Background: Cancer stem cells are presumed to have virtually unlimited proliferative and self-renewal abilities and to be highly resistant to chemotherapy, a feature that is associated with overexpression of ATP-binding cassette transporters. We investigated whether prolonged continuous selection of cells for drug resistance enriches cultures for cancer stem-like cells.
Publication Title
Prolonged drug selection of breast cancer cells and enrichment of cancer stem cell characteristics.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 48 Downloadable Samples
- Illumina mouseRef-8 v1.1 expression beadchip
Description
Background: Friedreich ataxia, an autosomal recessive neurodegenerative and cardiac disease, is caused by abnormally low levels of frataxin, an essential mitochondrial protein. All Friedreich ataxia patients carry a GAA/TTC repeat expansion in the first intron of the frataxin gene, either in the homozygous state or in compound heterozygosity with other loss-of-function mutations. The GAA expansion inhibits frataxin expression through a heterochromatin-mediated repression mechanism. Histone modifications that are characteristic of silenced genes in heterochromatic regions occur at expanded alleles in cells from Friedreich ataxia patients, including increased trimethylation of histone H3 at lysine 9 and hypoacetylation of histones H3 and H4.
Publication Title
HDAC inhibitors correct frataxin deficiency in a Friedreich ataxia mouse model.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Streptococcus suis is a major swine pathogen that can be transmitted to humans causing severe symptoms. A large human outbreak was described in China, where approximately 25% out of 215 infected humans developed an unusual streptococcal toxic shock-like syndrome (STSLS). Albeit increased expression of inflammatory mediators following infection by the Chinese S. suis strain was suggested as responsible for STSLS case severity, the mechanisms involved are still poorly understood. In this study, we investigated the host innate immune response to infection by either one of 3 strains of S. suis: 89-1591 (Canadian, intermediate virulence), P1/7 (European, high virulence), and SC84 (Chinese, epidemic strain). Using Illumina microarray and validating those results with qPCR and Luminex assay, infected mice showed elevated expression of mainly pro-inflammatory chemokine and cytokine genes. Generally, pro-inflammatory genes were expressed at a higher level in mice infected with S. suis strain SC84 > P1/7 > 89-1591. Interestingly, IFN was expressed at much higher levels only in mice infected with the S. suis strain SC84, which could potentially explain some of the STSLS symptoms. IFN-KO mice infected with SC84 showed better survival than WT mice while no differences was seen in mice infected with highly virulent P1/7 strain. Overall, our results show an important role of IFN in S. suis infections and might explain in part the increased virulence of SC84 responsible for a recent outbreak in China.
Publication Title
Exacerbated type II interferon response drives hypervirulence and toxic shock by an emergent epidemic strain of Streptococcus suis.
Sample Metadata Fields
Sex, Specimen part
View Samples