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GSE34093
Mus musculus
10 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The male germ cell gene regulator CTCFL is functionally different from CTCF and binds CTCF-like consensus sites in a nucleosome composition-dependent manner.
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Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
Description
The effect of CTCFL mutation on the transcriptional program in testes
Publication Title
The male germ cell gene regulator CTCFL is functionally different from CTCF and binds CTCF-like consensus sites in a nucleosome composition-dependent manner.
Alternate Accession IDs
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Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Sox9 Controls Self-Renewal of Oncogene Targeted Cells and Links Tumor Initiation and Invasion.
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Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
Description
Sox9 is a transcription factor expressed in most solid tumors. However, the molecular mechanisms underlying Sox9 function during tumorigenesis remain unclear. Here, using a genetic mouse model of basal cell carcinoma (BCC), the most frequent cancer in human, we show that Sox9 is expressed from the earliest step of tumor formation in a Wnt/-catenin dependent manner. Deletion of Sox9 together with the constitutive activation of Hedgehog (HH) signaling completely prevents BCC formation and leads to a progressive loss of oncogene expressing cells. Transcriptional profiling of oncogene expressing cells with Sox9 deletion, combined with in vivo ChIP-sequencing uncovers a cancer-specific gene network regulated by Sox9 that promotes stemness, extracellular matrix (ECM) deposition and cytoskeleton remodeling while repressing epidermal differentiation. Our study identifies the molecular mechanisms regulated by Sox9 that links tumor initiation and invasion.
Publication Title
Sox9 Controls Self-Renewal of Oncogene Targeted Cells and Links Tumor Initiation and Invasion.
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Specimen part
View Samples- Mus musculus
- 20 Downloadable Samples
Description
The C57BL/6.NOD-Aec1Aec2 mouse is a model for primary Sjgrens syndrome and was constructed by introducing two genetic intervals derived from the NOD mouse that confers Sjgrens syndrome (SjS)-like disease in SjS-non-susceptible C57BL/6 mice.
Publication Title
Transcriptional landscapes of emerging autoimmunity: transient aberrations in the targeted tissue's extracellular milieu precede immune responses in Sjögren's syndrome.
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Sex, Age, Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
Description
The transcriptomic changes induced in primary mouse hepatocytes (C57BL/6 ) by 7M of cisplatin after treatment for 24 and 48h
Publication Title
Characterisation of cisplatin-induced transcriptomics responses in primary mouse hepatocytes, HepG2 cells and mouse embryonic stem cells shows conservation of regulating transcription factor networks.
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Cell line, Treatment, Time
View Samples- Mus musculus
- 5 Downloadable Samples
Description
DREAM/KChIP-3 is a calcium-dependent transcriptional repressor highly expressed in immune cells. Transgenic mice expressing a dominant active DREAM mutant show reduced serum immunoglobulin levels. In vitro assays show that reduced immunoglobulin secretion is an intrinsic defect of transgenic B cells that occurs without impairment in plasma cell differentiation but with an accelerated entry in cell division and an increase in class switch recombination. B cells from DREAM knockout mice did not show any phenotype, due to compensation by endogenous KChIP-2. Expression arrays revealed modified expression of Edem1 and Derlin3, two proteins related to the ER-associated degradation pathway and of Klf9, a cell-cycle regulator. Our results disclose a function of DREAM and KChIP-2 in Ig subclass production in B lymphocytes.
Publication Title
Increased B cell proliferation and reduced Ig production in DREAM transgenic mice.
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Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
Description
Better understanding alveolarization mechanisms could help improving prevention and treatment of diseases characterized by reduced alveolar number, especially bronchopulmonary dysplasia (BPD). Although signaling through fibroblast growth factor (FGF) receptors is essential for alveolarization, involved ligands are unidentified. FGF18 whose expression peaks during alveolar septation is likely to be involved. Herein, a mouse model of inducible, lung-targeted FGF18-transgene was used to advance the onset of FGF18 expression, and genome-wide expression changes were determined.
Publication Title
Profiling target genes of FGF18 in the postnatal mouse lung: possible relevance for alveolar development.
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Specimen part, Disease
View Samples- Mus musculus
- 5 Downloadable Samples
Description
Homologue of Enhancer-of-split 1 (Hes1) is a transcription factor that regulates neuronal plasticity, promoting the growth of dendrites and increasing the GABAergic input. A higher expression of Hes1 also results in neuronal resistance against the noxious activity of amyloid beta, the main agent in the advent and progression of the Alzheimer's disease. As a transcription factor, Hes1 controls de expression of many genes. Using the microarray technology we have detected that the expression of one secreted synaptic protein, cerebellin 4 (Cbln4) was particularly increased upon overexpression of Hes1. We also present evidence that Cbln4 plays an essential role in the formation and maintenance of inhibitory GABAergic connections and that either overexpression of Cbln4 in cultured hippocampal neurons or the application of recombinant Cbln4 to the cultures increased the number of GABAergic varicosities and rescued neurons from amyloid beta induced cell death.
Publication Title
Cerebellin 4, a synaptic protein, enhances inhibitory activity and resistance of neurons to amyloid-β toxicity.
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Specimen part
View Samples- Mus musculus
- 22 Downloadable Samples
Description
Murine GVH-SSc dorsal scapular skin samples were analyzed to determine the effect of IFNAR-1 inhibition on gene expression at day 14 and day 28. Gene expression in GVH-SSc skin from mice treated with a neutralizing IFNAR-1 antibody was compared to that in GVH-SSc skin from mice treated with isotype IgG, with skin from syngeneic graft controls as reference.
Publication Title
Type I IFNs Regulate Inflammation, Vasculopathy, and Fibrosis in Chronic Cutaneous Graft-versus-Host Disease.
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Sex
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