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GSE44234
Drosophila melanogaster
12 Downloadable Samples
Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Innate immune responses rely on expression of potent effector molecules, such as antimicrobial peptides, which have the capability to kill invading microorganisms. The presence and recognition of microbial components triggers several signaling pathways, such as the Toll and IMD pathways, which in turn activate NF-kB/Rel transcription factors to induce transcription of a large number of immune system genes. Not much is known how these genes are kept silent in healthy flies in the presence of commensal microorganisms, and how the expression of immune defense genes is turned off. We found that several immune defense genes are constitutively active in nub[1] mutants, indicating that the POU domain transcription factor Pdm1/Nubbin may act as a repressor of immune gene expression.
Publication Title
The Oct1 homolog Nubbin is a repressor of NF-κB-dependent immune gene expression that increases the tolerance to gut microbiota.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 16 Downloadable Samples
IlluminaHiSeq2000
Description
DNA methylation is thought to induce a transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators that do not recognize their binding sites when methylated, and the recruitment of transcriptional repressors that specifically bind methylated DNA. Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. However, the exact contribution of each protein in the DNA methylation dependent transcriptional repression occurring during development and diseases remains elusive. Here we present MBD2 ChIPseq data generated from the endogenous protein in an isogenic cellular model of human mammary oncogenic transformation. In immortalized or transformed cells, MBD2 was found in one fourth of methylated regions and associated with transcriptional silencing. Depletion of MBD2 induces upregulations of genes bound by MBD2 and methylated in their transcriptional start site regions. MBD2 was partially redistributed on methylated DNA during oncogenic transformation, independently of DNA methylation changes. Genes downregulated during this transformation preferentially gained MBD2 binding sites on their promoter. Depletion of MBD2 in transformed cells induced the upregulation of some of these repressed genes, independently of the strategy used for the abrogation of oncosuppressive barriers. Our data confirm that MBD2 is a major interpret of DNA methylation, and show an unreported dynamic in this interpretation during oncogenic transformation. Overall design: RNAseq of untreated HMEC-hTERT cells, siCtrl, siMBD2 or DAC treated HMLER cells, siCtrl or siMBD2 treated HME-ZEB1-RAS and HME-shP53-RAS cells, in duplicates.
Publication Title
Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina HiSeq 2500
Description
In order to determine the imprinted transcription factor Zac1 targets, we overexpressed Zac1 in a mouse insulinoma cell line and measured the regulated expressed genes by RNA-seq. We have shown that Zac1 regulates many genes belonging to the Imprinted Gene Network, including genes coding for the extra-cellular matrix. Overall design: Determination of Zac1 target genes in transfected Min6 cells (4 biological replicates) using RNA-seq, .
Publication Title
Identification of Plagl1/Zac1 binding sites and target genes establishes its role in the regulation of extracellular matrix genes and the imprinted gene network.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 104 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Clinical heterogeneity of esrtrogen receptor-negative, progesterone receptor-negative [ER(-)/PR(-)] breast cancer (BC) suggests biological heterogeneity. We performed gene expression analysis of primary BCs and BC cell lines to identify the underlying biology of ER(-)/PR(-) disease, define subsets, and identify potential therapeutic targets.
Publication Title
An estrogen receptor-negative breast cancer subset characterized by a hormonally regulated transcriptional program and response to androgen.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples- Macaca mulatta
- 32 Downloadable Samples
- Affymetrix Rhesus Macaque Genome Array (rhesus)
Description
The mucosa that lines the respiratory and gastrointestinal (GI) tracts is an important portal of entry for pathogens and provides the frontline of immune defense against HIV infection. Using the simian immunodeficiency virus (SIV) rhesus macaque model, we have performed a comparative analysis of host gene expression in the lung and GI mucosa in response to SIV infection and antiretroviral therapy.
Publication Title
Enhanced innate antiviral gene expression, IFN-α, and cytolytic responses are predictive of mucosal immune recovery during simian immunodeficiency virus infection.
Sample Metadata Fields
Specimen part
View Samples- Macaca mulatta, Homo sapiens
- 13 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Cell line, Treatment
View Samples- Macaca mulatta
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
A majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the potential of simian immunodeficiency virus (SIV) infected rhesus macaques to serve as a non-human primate model for oral manifestations of HIV disease.
Publication Title
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Macaca mulatta
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
A majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the potential of simian immunodeficiency virus (SIV) infected rhesus macaques to serve as a non-human primate model for oral manifestations of HIV disease.
Publication Title
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 1 Downloadable Sample
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
A majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the impact of chronic exposure to the pro-inflammatory cytokine, interferon gamma, on the growth and barrier functions of the oral epithelium.
Publication Title
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
We are investigating the transcriptional response of changes in RNA steady-state levels between normal and DM1.
Publication Title
RNA steady-state defects in myotonic dystrophy are linked to nuclear exclusion of SHARP.
Sample Metadata Fields
Specimen part
View Samples