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GSE99035
Mus musculus
12 Downloadable Samples
Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MGAT1 and Complex N-Glycans Regulate ERK Signaling During Spermatogenesis.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Loss of Mgat1 in spermatogonia was investigated in germ cells from 23 day males. Gene expression changes induced by deletion of Mgat1 were determined using the Affymetrix GeneChip Mouse Gene 2.0 ST Array.
Publication Title
MGAT1 and Complex N-Glycans Regulate ERK Signaling During Spermatogenesis.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Mechanistic insights into MGAT1 loss during spermatogenesis were investigated in germ cells from 22 day males. Gene expression changes induced by deletion of Mgat 1in spermatogonia were determined using the Affymetrix GeneChip Whole Transcript Plus Reagent Kit.
Publication Title
MGAT1 and Complex N-Glycans Regulate ERK Signaling During Spermatogenesis.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Mouse ES cells were differentiated for 6 days. Undifferentiated cells (d0) were compared to cells harvested at 24 hour timepoints (d1-d6).
Publication Title
Transcriptional profiling of mouse and human ES cells identifies SLAIN1, a novel stem cell gene.
Sample Metadata Fields
Age, Specimen part, Cell line, Time
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133B Array (hgu133b), Affymetrix Human Genome U133A Array (hgu133a)
Description
Undifferentiated cells of different passage numbers (p19 and p128) were compared to cells differentiated in hanging drops for 5 days (d5 embryoid bodies) or expanded on gelatin coated dishes for a further 9 days (d14 embryoid bodies).
Publication Title
Transcriptional profiling of mouse and human ES cells identifies SLAIN1, a novel stem cell gene.
Sample Metadata Fields
Age, Specimen part, Cell line, Time
View Samples- Mus musculus
- 32 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Macrophage polarization between the M2 (repair, pro-tumorigenic) and M1 (inflammatory) phenotypes is seen as a continuum of states. The detailed transcriptional events and signals downstream of CSF-1R that contribute to amplification of the M2 phenotype and suppression of the M1 phenotype are largely unknown. Macrophage CSF-1R pTyr-721 signaling promotes cell motility and enhancement of tumor cell invasion in vitro. Combining analysis of cellular systems for CSF-1R gain-of-function and loss-of-function with bioinformatic analysis of the macrophage CSF-1R pTyr-721-regulated transcriptome, we uncovered miR-21 as a downstream molecular switch controlling macrophage activation and identified ERK1/2 and NF-B as CSF-1R pTyr-721-regulated signaling nodes. We show that CSF-1R pTyr-721 signaling suppresses the proinflammatory phenotype, predominantly by induction of miR-21. Profiling of the miR-21-regulated mRNAs revealed that 80% of the CSF-1-regulated canonical miR-21 targets are pro-inflammatory molecules. Additionally, miR-21 positively regulates M2 marker expression. Moreover, miR-21 feeds back to positively regulate its own expression and to limit CSF-1R-mediated activation of ERK1/2 and NF-B. Consistent with an anti-inflammatory role of miRNA-21, intraperitoneal injection of mice with a miRNA-21 inhibitor increases the recruitment of inflammatory monocytes and enhances the peritoneal monocyte/macrophage response to lipopolysaccharide (LPS).
Publication Title
Colony stimulating factor-1 receptor signaling networks inhibit mouse macrophage inflammatory responses by induction of microRNA-21.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Rattus norvegicus
- 19 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
In the present study, microarray analysis was performed on RNA isolated from purified SLCs, PLCs, ILCs, ALCs and bone stem cells, using Affymetrix Rat Genome RAE230 2.0 arrays which monitor ~30,000 transcripts from over ~28,000 well-substantiated genes. The focus is on the differences and similarities between SLCs and bone stem cells, and between SLCs and PLCs, ILCs and ALCs
Publication Title
Stem Leydig cell differentiation: gene expression during development of the adult rat population of Leydig cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
to analyse the transcriptomic response of human intestinal tissue engrafted in SCID mice to Shigella infection
Publication Title
Virulent Shigella flexneri subverts the host innate immune response through manipulation of antimicrobial peptide gene expression.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Integration of high-risk human papillomavirus (HRHPV) into the host genome is a key event in cervical neoplastic progression. Integration is associated with deregulated expression of the viral oncogenes E6 and E7 and acquisition of a selective growth advantage for cells containing integrants. Overexpression of the viral transcriptional regulator E2 from heterologous promoters has an inhibitory effect on transcription from integrated HRHPV. We therefore hypothesised that loss of E2-expressing episomes from cells in which integration had previously occurred would be required for such cells to gain a growth advantage. Using the unique W12 model of cervical squamous carcinogenesis, we show that cells containing integrated HPV16 reproducibly emerged during long-term culture when there had been a rapid fall in episome numbers. During the period of emergence it is possible to isolate single-cell clones containing an intracellular mixture of the integrant being selected and episomes at reduced load. Microarray analysis showed that episome loss was closely associated with endogenous activation of antiviral response genes that are also inducible by the type I interferon (IFN) pathway. Taken together, our results indicate that episome loss, associated with induction of antiviral response genes, is a key event in the spontaneous selection of cervical keratinocytes containing integrated HPV16. We conclude that cervical carcinogenesis requires not only HRHPV integration, but also loss of inhibitory episomes.
Publication Title
Selection of cervical keratinocytes containing integrated HPV16 associates with episome loss and an endogenous antiviral response.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 21 Downloadable Samples
Description
Human embryonic stem cells (hESCs) were specified as ventral telencephalic neuroectoderm (day 4) and then into medial ganglionic emininence (MGE)-like progenitors (day 15) and were subsequently differentiated into cortical interneuron (cIN)-like cells (day 25-35), by modification of previously published protocols. RNA-seq analysis at days 0, 4, 15, 25, and 35 defined transcriptome signatures for MGE and cIN cell identity. Further integration of these gene expression signatures with ChIP-seq for the NKX2-1 transcription factor in MGE-like progenitors defined NKX2-1 putative direct targets, including genes involved in both MGE specification and in several aspects of later cIN differentiation (migration, synaptic function). Among the NKX2-1 direct targets with MGE and cIN enriched expression was CHD2, a chromatin remodeling protein. Since CHD2 haploinsufficiency can cause epilepsy and/or autism, which can involve altered cIN development or function, we evaluated CHD2 requirements in these processes. Transcriptome changes were evaluated in CHD2 knockdown MGE-like progenitors at day 15, revealing diminished expression of genes involved in MGE specification and cIN differentiation including channel and synaptic genes implicated in epilepsy, while later cIN electrophysiological properties were also altered. We defined some shared cis-regulatory elements bound by both NKX2-1 and CHD2 and characterized their ability to cooperatively regulate cIN gene transcription through these elements. We used these data to construct regulatory networks underlying MGE specification and cIN differentiation and to define requirements for CHD2 and its ability to cofunction with NKX2-1 in this process. Overall design: To comprehensively define changes in gene expression profiles that accompany cortical interneuron (cIN) specification and differentiation process, we have performed RNA sequencing analysis at days 0 (hESCs), 4, 15, 25, and 35. To understand the gene regulatory networks through which NKX2-1 may directly control these processes, we defined its direct targets by performing NKX2-1 ChIP-seq in day 15 MGE-like cells. Chromatin enrichment for NKX2-1 binding was compared to input and IgG controls. To define the CHD2-dependent gene expression programs during cIN specification, we used CHD2 knockdown (KD) to conduct RNA-seq analysis in d15 CHD2 KD MGE-like cells.
Publication Title
Regulatory networks specifying cortical interneurons from human embryonic stem cells reveal roles for CHD2 in interneuron development.
Sample Metadata Fields
No sample metadata fields
View Samples