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SRP055777
Mus musculus
22 Downloadable Samples
Illumina HiSeq 2000
Description
PDGF and FGF treatment in E13.5 MEPMs. 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates) Overall design: 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates)
Publication Title
Receptor tyrosine kinases modulate distinct transcriptional programs by differential usage of intracellular pathways.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 11 Downloadable Samples
- Illumina HiSeq 2000, Illumina Genome Analyzer IIx
Description
Receptor tyrosine kinase signaling is critical for mammalian craniofacial development, but the key downstream transcriptional effectors remain unknown. We demonstrate that SRF is induced by both PDGF and FGF signaling in mouse embryonic palatal mesenchyme cells, and Srf neural crest conditional mutants exhibit facial clefting accompanied by proliferation and migration defects. Srf and Pdgfra mutants interact genetically in craniofacial development, but Srf and Fgfr1 mutants do not. This signal specificity is recapitulated at the level of cofactor activation: while both PDGF and FGF target gene promoters show enriched genome-wide overlap with SRF ChIP-seq peaks, PDGF selectively activates a network of MRTF-dependent cytoskeletal genes. Collectively, our results identify a novel role for SRF in proliferation and migration during craniofacial development and delineate a mechanism of receptor tyrosine kinase specificity mediated through differential cofactor usage, leading to a unique PDGF-responsive SRF-driven transcriptional program in the midface. Overall design: Serum Starved MEPMs (4 replicates), 1 hr PDGF treated MEPMs (4 replicates), 1 hr FGF treated MEPMs (3 replicates)
Publication Title
Receptor tyrosine kinases modulate distinct transcriptional programs by differential usage of intracellular pathways.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip
Description
Women are born with millions of primordial follicles which gradually decrease with increasing age and this irreversible supply of follicles completely exhausts at menopause. The fertility capacity of women diminishes in parallel with aging. The mechanisms for reproductive aging are not fully understood. In our recent work we observed a decline in BRCA1 mediated DNA repair in aging rat primordial follicles. To further understand the age-related molecular changes, we performed microarray gene expression analysis using total RNA extracted from immature (1820 days) and aged (400450 days) rat primordial follicles. The results of current microarray study revealed that there were 1011 (>1.5 fold, p<0.05) genes differentially expressed between two groups in which 422 genes were up-regulated and 589 genes were down-regulated in aged rat primordial follicles compared to immature. The gene ontology and pathway analysis of differentially expressed genes revealed a critical biological function such as cell cycle, oocyte meiosis, chromosomal stability, transcriptional activity, DNA replication and DNA repair were affected by age and this considerable difference in gene expression profiles may have adverse influence on oocyte quality. Our data provide information on the processes that may contribute to aging and age-related decline in fertility.
Publication Title
Age-related changes in gene expression patterns of immature and aged rat primordial follicles.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene Expression Array (primeview), Illumina HiSeq 2000
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Nitric Oxide Regulates Gene Expression in Cancers by Controlling Histone Posttranslational Modifications.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Epigenetic response in mice mastitis: Role of histone H3 acetylation and microRNA(s) in the regulation of host inflammatory gene expression during Staphylococcus aureus infection.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Bacterial infection in the mammary gland parenchyma induces local inflammation that can lead to a multietiological complex disease called mastitis. Globally Staphylococcus aureus is the single largest mastitis pathogen and the infection can ultimately result in either subclinical or chronic and sometimes lifelong infection. In the present report we have addressed the differential inflammatory response in the mice mammary tissue during intramammary infection and the altered epigenetic context induced by two closely related strains of S. aureus. Immunohistochemical and immunoblot analysis showed strain specific hyperacetylation at histone H3K9 and H3K14 residues. Real-time PCR and genome-wide gene expression studied showed expression of a set of proinflammatory genes and cytokines in a temporal manner. Remarkably, over expression of the genes significantly correlated with the promoter specific acetylation in these residues. Furthermore, we have identified several differentially expressed known miRNAs and 4 novel miRNAs in the S. aureus infected mice mammary tissue by small RNA sequencing. By employing these gene expression data, an attempt has been made to delineate the gene regulatory networks in the strain specific inflammatory response. Apparently, one of the isolates of S. aureus activated the NFkB signaling leading to drastic inflammatory response and induction of immune surveillance, which could lead to rapid clearance of the pathogen. The other strain repressed most of the inflammatory response, which might help in its sustenance in the host tissue. Taken together, our studies shed substantial lights to understand the mechanisms of strain specific differential inflammatory response to S. aureus infection during mastitis.
Publication Title
Epigenetic response in mice mastitis: Role of histone H3 acetylation and microRNA(s) in the regulation of host inflammatory gene expression during Staphylococcus aureus infection.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
miRNA abnormalities are increasingly relevent to cancer development, We used microarrays to detail the global programme of gene expression upon miR-483 overexpression in sarcoma cell line MHH-ES-1.
Publication Title
The IGF2 intronic miR-483 selectively enhances transcription from IGF2 fetal promoters and enhances tumorigenesis.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 1 Downloadable Sample
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
MicroRNAs predominantly decrease gene expression; however, specific mRNAs are translationally upregulated in quiescent (G0) mammalian cells and immature Xenopus laevis oocytes by an FXR1a-associated microRNP (microRNA-protein complex) that lacks the microRNP repressor, GW182. We conducted global proteomic analysis in THP1 cells depleted of FXR1 to globally identify activation targets of more than one microRNA, since FXR1 is required for microRNAmediated translation activation in THP1 G0 cells by FXR1-microRNPs.Since proteomic data changes could also be due to changes at the RNA level, total RNA levels in FXR1knockdown compared to control shRNA cells were examined in parallel by microarray analysis using Affymetrix Human GeneChip 2.0 ST.
Publication Title
A Specialized Mechanism of Translation Mediated by FXR1a-Associated MicroRNP in Cellular Quiescence.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 11 Downloadable Samples
- Illumina HiSeq 2500
Description
Mononuclear phagocytes are a diverse cell family that occupy all tissues and assume numerous functions to support tissue and systemic homeostasis. Our ability to investigate the roles of individual subsets is limited by an absence of approaches to ablate gene function within specific sub-populations. Using Nr4a1-dependent Ly6Clow monocytes as a representative cell type we show that enhancer deletion addresses these limitations. Combining ChIP-Seq and molecular approaches we identify a single, conserved, sub-domain within the Nr4a1 enhancer that is essential for Ly6Clow monocyte development. Mice lacking this enhancer lack Ly6Clow monocytes but retain Nr4a1 gene expression in macrophages during steady state and in response to LPS. Nr4a1 is a key negative regulator of inflammatory gene expression and decoupling these processes allows Ly6Clow monocytes to be studied without confounding influences. Enhancer targeting possesses greater specificity than cre recombinase-mediated gene deletion, providing a route to generate loss-of-function models in closely related cell types. Overall design: Paired End mRNA sequencing of FACS purified primary murine MDP, cMoP, Ly6Chi and Ly6Clow monocytes from the bone marrow and Ly6Chi and Ly6Clow monocytes from the peripheral blood
Publication Title
Deleting an Nr4a1 Super-Enhancer Subdomain Ablates Ly6C<sup>low</sup> Monocytes while Preserving Macrophage Gene Function.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus, Homo sapiens
- 30 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
MicroRNAs have emerged as major genetic elements in the genesis and suppression of cancer. Here, multi-dimensional cancer genome analysis and validation has defined a novel Glioblastoma Multiforme (GBM) tumor suppressor pathway and mechanism of action centered on Quaking (QK), a member of the STAR family of RNA-binding proteins. Combined functional, biochemical and computational studies establish that p53 directly regulates QK gene expression, QK protein binds and stabilizes miR-20a of the cancer-relevant miR-17-92 cluster, and miR-20a in turn functions to regulate TGFR2 and the TGF signaling network. Linkage of these pathway components is supported by their genome and expression status across GBM specimens and by their gain- and loss-of-function interactions in in vitro and in vivo complementation studies. This p53-QK-miR-20a axis expands our understanding of the p53 tumor suppression network in cancer and reveals a novel tumor suppression mechanism involving regulation of specific cancer-relevant microRNAs.
Publication Title
STAR RNA-binding protein Quaking suppresses cancer via stabilization of specific miRNA.
Sample Metadata Fields
Specimen part, Cell line
View Samples