Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Co-expression networks in generation of induced pluripotent stem cells

ABSTRACT: We developed an adenoviral vector, in which Yamanakaâ??s four reprogramming factors (RFs) were controlled by individual CMV promoters in a single cassette (Ad-GFP-SOcMK). This permitted coordinated expression of RFs (SOX2, OCT3/4, c-MYC and KLF4) in a cell for a transient period of time, synchronizing the reprogramming process with the majority of transduced cells assuming induced pluripotent stem cell (iPSC)-like characteristics as early as 3 days. These reprogrammed cells resembled human ES cells with regard to morphology, biomarker expression, and could be differentiated into cells of the germ layers in vitro and in vivo. These iPSC-like cells, however, failed to expand into larger iPSC colonies. The short and synchronized reprogramming process allowed us to study global transcription changes within short time intervals. Weighted Gene Co-Expression Network analysis (WGCNA) identified sixteen large gene co-expression modules, each including members of gene ontology categories involved in cell differentiation and development. In particular, the brown module contained a significant number of ES cell marker genes, whereas the turquoise module contained cell-cycle related genes that were downregulated in contrast to upregulation in human ESCs. Strong coordinated expression of all 4 RFs via adenoviral transduction may constrain stochastic processes and lead to silencing of genes important for cellular proliferation. Cells were dedifferentiated and gene expression assessed at 13 timepoints

ORGANISM(S): Homo sapiens

SUBMITTER: Giovanni Coppola

PROVIDER: E-GEOD-72676 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Co-expression networks in generation of induced pluripotent stem cells

Project description:We developed an adenoviral vector, in which Yamanaka’s four reprogramming factors (RFs) were controlled by individual CMV promoters in a single cassette (Ad-GFP-SOcMK). This permitted coordinated expression of RFs (SOX2, OCT3/4, c-MYC and KLF4) in a cell for a transient period of time, synchronizing the reprogramming process with the majority of transduced cells assuming induced pluripotent stem cell (iPSC)-like characteristics as early as 3 days. These reprogrammed cells resembled human ES cells with regard to morphology, biomarker expression, and could be differentiated into cells of the germ layers in vitro and in vivo. These iPSC-like cells, however, failed to expand into larger iPSC colonies. The short and synchronized reprogramming process allowed us to study global transcription changes within short time intervals. Weighted Gene Co-Expression Network analysis (WGCNA) identified sixteen large gene co-expression modules, each including members of gene ontology categories involved in cell differentiation and development. In particular, the brown module contained a significant number of ES cell marker genes, whereas the turquoise module contained cell-cycle related genes that were downregulated in contrast to upregulation in human ESCs. Strong coordinated expression of all 4 RFs via adenoviral transduction may constrain stochastic processes and lead to silencing of genes important for cellular proliferation.

2016-03-01 | GSE72676 | GEO

The RON receptor tyrosine kinase promotes metastasis by triggering epigenetic reprogramming through the thymine glycosylase MBD4 (gene expression array)

Project description:Metastasis is the major cause of death in cancer patients, yet the genetic/epigenetic programs that drive metastasis are poorly understood. Here, we report a novel epigenetic reprogramming pathway that is required for breast cancer metastasis. Concerted differential DNA methylation is initiated by activation of the RON receptor tyrosine kinase by its ligand, macrophage stimulating protein (MSP). Through PI3K signaling, RON/MSP promotes expression of the G:T mismatch-specific thymine glycosylase MBD4. RON/MSP and MBD4-dependent aberrant DNA methylation results in misregulation of a specific set of genes. Knockdown of MBD4 reverses methylation at these specific loci, and blocks metastasis. We also show that the MBD4 glycosylase catalytic residue is required for RON/MSP-driven metastasis. Analysis of human breast cancers revealed that this epigenetic program is significantly associated with poor clinical outcome. Furthermore, inhibition of Ron kinase activity with a new pharmacological agent blocks metastasis of patient-derived breast tumor grafts in vivo. To determine the molecular mechanisms by which RON/MSP drives breast cancer metastasis, we performed microarray gene expression profiling of MCF7, MCF7-RON/MSP and MCF7-RON/MSP-shMBD4 cells.

2014-01-02 | E-GEOD-52567 | biostudies-arrayexpress

Microarray experment to identify genes differentially expressed in the DDT resistant 91R strain of Drosophila

Project description:Transcriptional profiling of mature adult 91R males compared to 91C males. RNA was extracted from mature adult 91R or 91C strain of Drosophila melanogaster and subjected to micraoarray analysis.

2014-08-31 | E-GEOD-48952 | biostudies-arrayexpress

Drosophila 16-20 hrs embryos: DHR3G60S/Df(2R)12 vs. w1118

Project description:Transcriptional profiling of 16-20 hrs Drosophila embryos comparing control (w1118) and DHR3 mutants (DHR3G60S/Df(2R)12) Two-condition experiment, control vs. DHR3 mutant embryos. Biological replicates: 4 replicates.

2010-05-19 | E-GEOD-18577 | biostudies-arrayexpress

Gene expression changes upon knockdown or over-expression of the ETS gene ETV4 in prostate cancer cell lines

Project description:Chromosomal abnormalities that give rise to elevated expression levels of the ETS genes ETV1, ETV4, ETV5, or ERG are prevalent in prostate cancer, but the function of these transcription factors in carcinogenesis is not clear. Previous work implicates ERG, ETV1, and ETV5 as regulators of invasive growth but not transformation in cell lines. Here we show that the PC3 prostate cancer cell line provides a model system to study the over-expression of ETV4. Anchorage independent growth assays and microarray analysis indicate that high ETV4 expression is critical for the transformation phenotype of PC3 cells. However, genes up-regulated upon ETV4 over-expression were very similar to genes up-regulated by ETV1 over-expression in the RWPE-1 normal prostate cell line. Together these data indicate that the ETV4 dependent transformation phenotype observed in PC3 cells is due to the genetic background of the cell line, rather than a distinct characteristic of ETV4. Furthermore, these findings suggest that the function of ETS genes in prostate cancer may differ based on other genetic alterations in a tumor. Two sets of two color experiments. First is PC3 cells expressing one of two independent ETV4 shRNAs versus PC3 cells expressing a control shRNA (luciferase). Second is RWPE-1 cells expressing 3xFlag tagged ETV4 versus RWPE-1 cells with a control (empty) vector.

2011-03-24 | E-GEOD-21209 | biostudies-arrayexpress

Expression profiling of DHR38-dependent transcripts in Drosophila larvae

Project description:Transcriptional profiling of Drosophila third instar larvae comparing control (w1118) and DHR38 mutants (DHR38Y214/Df(2)KetelRX32) Two-condition experiment, control vs. DHR38 mutant larvae. Biological replicates: 3 replicates.

2010-12-01 | E-GEOD-23047 | biostudies-arrayexpress

BxPC-3 cells: growth in different nutrients

Project description:The MondoA transcription factor forms a heterocomplex with its obligate partner Mlx to regulate ~75% of glucose-dependent transcription. By mediating glucose-induced activation of thioredoxin-interacting protein (TXNIP), MondoA directly represses glucose uptake. Given the predominant role of MondoA in controlling glucose-dependent transcription and glucose uptake, we asked whether glutamine regulates MondoA activity. Expression profiles from glucose and glutamine starved BxPC-3 cells (-G-Q) were compared with those from cells grown in glucose only (+G-Q), glutamine only (-G+Q) or glucose plus glutamine (+G+Q). As expected, TXNIP expression was highly induced by glucose. However, the addition of glutamine repressed the glucose-dependent induction of TXNIP. We show that glutamine inhibits MondoA-dependent transcriptional activation of TXNIP by triggering the recruitment of a histone deacetylase-dependent corepressor to the amino terminus of MondoA. Consistent with the repression of TXNIP, glucose uptake is elevated in cells grown in the presence of glucose and glutamine. Finally, alpha-ketoglutarate, a tricarboxylic acid cycle intermediate, also blocks MondoA-dependent activation of TXNIP and stimulates glucose uptake. Together, these results suggest that glutamine-dependent mitochondrial anapleurosis stimulates glucose uptake by restricting TXNIP expression via MondoA:Mlx complexes. Four growth conditons; four biological replicates

2010-08-18 | E-GEOD-17632 | biostudies-arrayexpress

Vitamin C Promotes Positive Selection of Mouse T Cells

Project description:We discovered that vitamin C (ascorbic acid) is required for differentiation of mouse bone marrow-derived progenitor cells in T cell cultures based on OP9-DL1 stromal cells. This microarray dataset evaluates differential expression of genes in OP9-DL1 stromal cells as well as in lymphocytes developing in the cultures when a stabilized form of ascorbic acid (l-ascorbic acid 2-phosphate; pAsc) is added. Cultures were maintained in the absence of pAsc for 13 days, at which time 800 micromolar pAsc was added. Cells were harvested after 24 and 72 hours (24 hours only in the case of OP9-DL1 cells) and solubilized in Trizol. Two-condition experiment, differentiating T lymphoid cells with or without pAsc, 2 timepoints, OP9-DL1 cells with or without pAsc, 1 timepoint, no technical replicates

2011-08-23 | E-GEOD-31596 | biostudies-arrayexpress

Gene expression in Tcf4Het ApcHet mouse colon tumors compared to normal colon

Project description:The Wnt/M-NM-2-catenin pathway plays multiple/diverse roles in development by regulating gene expression via Tcf/Lef DNA binding factors. Misregulation of this pathway is thought to initiate colon adenoma formation. It is controversial whether Tcf4 (Tcf7L2) functions as an oncogene or tumor suppressor gene in colon carcinogenesis. We show here that Tcf4 haploinsufficiency results in colon tumor formation in a mouse tumor model that normally only develops small intestinal tumors. Further, we show that loss of Tcf4 early in development and in adult colon results in increased cell proliferation. These findings strongly suggest that Tcf4 normally modulates proliferation of the colonic epithelium and that disruption of Tcf4 activity increases proliferation leading to colon tumorigenesis. Taken together our in vivo studies favor a tumor suppressor function for Tcf4. 4 Normal Colon and 4 colon tumor from independent mouse tissue samples

2011-03-15 | E-GEOD-27522 | biostudies-arrayexpress

Microarray experiment to identify gene expression changes in response to Phenobarbital treatment and CncC overexpression in Drosophila.

Project description:Transcriptional profiling of mature adult w1118 males treated with phenobarbital compared to controls and heat treated HS-CncC flies compared with heat treated w1118 flies. Mature adult w1118 males were treated witheither 5% sucrose alone or 5% sucrose supplemented with 0.3% phenobarbital for six hours, following which RNA was extracted and subjected to micraoarray analysis.Similarly,mature adult w1118 flies or HS-CncC flies were subjected to heat treatment at 37oC for 30 minutes and recovered at room temperature for two hours,after which RNA was exctracted and subjected to microarray analysis.

2011-11-29 | E-GEOD-30087 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data