This SuperSeries is composed of the SubSeries listed below.
ChIP-seq reveals cell type-specific binding patterns of BMP-specific Smads and a novel binding motif.
Specimen part, Cell line, Treatment
View SamplesSmad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing.
ChIP-seq reveals cell type-specific binding patterns of BMP-specific Smads and a novel binding motif.
Specimen part, Treatment
View SamplesSmad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions.
ChIP-seq reveals cell type-specific binding patterns of BMP-specific Smads and a novel binding motif.
Specimen part, Treatment
View SamplesCarrying out both RNA-seq and Smad1/5 genome-wide chromatin immunoprecipitation and sequencing (ChIP-seq) analyses of mESCs in the naïve or primed states, we revisit the roles of BMP signaling in mESCs. Overall design: RNA-seq analysis in 2 cell types; mESCs and ES-derived EpiSC (ESD-EpiSCs).
BMP Sustains Embryonic Stem Cell Self-Renewal through Distinct Functions of Different Krüppel-like Factors.
No sample metadata fields
View SamplesAims: establishment of reference samples to investigate gene expression selective for endocrine or ductal-exocrine cells within the adult human pancreas. To this end, human islet endocrine cells, FACS-enriched in insulin+ cells, (n=3) and human exocrine ductal cells (n=2) are compared on Affymetrix HG133A platform with duplicate hybridizations of a panel of other primary human tissues.
Clusters of conserved beta cell marker genes for assessment of beta cell phenotype.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Ras and TGF-β signaling enhance cancer progression by promoting the ΔNp63 transcriptional program.
Specimen part, Cell line
View SamplesWe demonstrate that activation of Ras and TGF- pathways strengthens the binding of p63 to its genomic sites and modulates the expression of p63 target genes.
Ras and TGF-β signaling enhance cancer progression by promoting the ΔNp63 transcriptional program.
Cell line
View SamplesThe study was designed to capture the in vivo adaptations of nutrient-sensing pancreatic beta cells to fed or fasted (24h) state.
Clusters of conserved beta cell marker genes for assessment of beta cell phenotype.
Sex, Age, Specimen part
View SamplesAbstract Two major dendritic cell (DC) subsets have been described in the islets of mice: The immunogenic CD8-CD11b+ DCs and the tolerogenic CD8+CD103+ DCs. We have recently reported on reduced numbers of the minor population of tolerogenic CD8+CD103+ DCs in the pancreas of 5 week old pre-diabetic non-obese diabetic (NOD) mice. Aim: To analyze also the larger subset of CD11c+CD8- DCs isolated from the pancreas of pre-diabetic NOD mice 1) for maturation and tolerance inducing molecules found abnormally expressed on CD8+CD103+ DCs, and 2) for genome-wide gene expression to further elucidate abnormalities in underlying gene expression networks. Methods: CD11c+CD8- DCs were isolated from 5 week old C57BL/6 and NOD pancreas. Expression of cell surface markers including CD86, CCR5, CD11b, CD103, Clec9a, CD24 and CD200R3 were measured by FACS. Genome-wide gene expression by microarray was assessed during the steady state and after in vitro LPS stimulation. Results: The steady state pancreatic CD11c+ CD8- DCs during the pre-diabetic stage showed: 1) A reduced expression of several gene networks important for the prime functions of the cell, such as for cell renewal, immune stimulation and immune tolerance induction, for migration and for the provision of growth factors for beta cell regeneration. This general deficiency state was corroborated by a reduced in vivo proliferation (BrdU incorporation) of the cells and the reduced expression in FACS analysis of CD86, CCR5, CD103, Clec9a, CD24 and CD200R3 on the cells. 2) A hyper reactivity of these cells to LPS correlated with an enhanced pro-inflammatory state characterized by altered expression of a number of classical pro-inflammatory factors and cytokines. Conclusion: The NOD CD11c+CD8- DCs seem to be Janus-faced depending on the conditions: Deficient in steady state with reduced immune stimulation capabilities also for tolerance induction; over-inflammatory with a molecular profile suggesting a preferential stimulatory capacity for Th1 cells when encountering a Pathogen-Associated Molecular Pattern (PAMP) in the form of LPS.
The gene expression profile of CD11c+ CD8α- dendritic cells in the pre-diabetic pancreas of the NOD mouse.
Sex, Age, Specimen part, Treatment
View SamplesThe Eol1 cell line has been derived from a patient with chronic eosiniphilic leukemia. Eol1 cells express the FIP1L1-PDGFRalpha oncogene. Inhibition of FIP1L1-PDGFRalpha with imatinib mesylate (Glivec) blocks proliferation and survival of the cells. We performed microarray expression analysis to identify genes specifically regulated by FIP1L1-PDGFRalpha using imatinib-treated cells as baseline. The list of regulated genes was consistent with the activation of STAT trancription factors by FIP1L1-PDGFRA.
Transcription factor regulation can be accurately predicted from the presence of target gene signatures in microarray gene expression data.
Cell line, Treatment
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