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

Transcription profiling of mouse ES cells treated by varying levels of activated Smad2/3 over time in the presence of protein synthesis

ABSTRACT: The tet-on system was activated by treatment of the cells with doxycycline (Dox) in concentrations 1 microgram per milliliter. The Smad2/3 phosphorylation was inhibited by treatment of the cells with SB-431542. The TAG1 cells were treated with SB inhibitor and Dox activator and samples were analyzed by microarrays (affymetrix) at different time points during this treatment.

ORGANISM(S): Mus musculus

SUBMITTER: Vasso Episkopou

PROVIDER: E-TABM-574 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Human somatic cell mutagenesis creates genetically tractable sarcomas

Project description:Creating spontaneous yet genetically tractable human tumors from normal cells presents a fundamental challenge. Retroviruses and transposons have been separately used as somatic cell insertional mutagens to identify cancer drivers in model organisms. Here we combined these mutagenic elements to enable cancer gene discovery starting with normal human cells. Lentivirus was used to seed gain- and loss-of-function gene disruption elements which were further deployed by Sleeping Beauty transposons throughout the genome of human bone explant mesenchymal cells. De novo tumors rapidly generated in this context were high-grade sarcomas corresponding to the spectrum of myxofibrosarcoma and undifferentiated pleomorphic sarcoma, aggressive neoplasms with a predilection for older adults. Tumor insertion sites were genome-wide and enriched in regions of recurrent somatic copy number alteration found in multiple cancers, with a bias towards those of sarcomas. Novel driver genes which sustain somatic alterations in cancer patients were pinpointed. We identify the gene HDLBP, which codes for the RNA binding protein vigilin, as a candidate tumor suppressor deleted at 2q37.3 in greater than one in ten tumors across multiple tissues of origin. Hybrid viral-transposon systems will accelerate the functional annotation of cancer genomes by enabling insertional mutagenesis screens in higher eukaryotes that are not amenable to germline transgenesis. Lentivirus was used to seed gain- and loss-of-function gene disruption elements which were further deployed by Sleeping Beauty (SB) transposons throughout the genome of human bone explant mesenchymal cells. Genomic locations of LV (lentiviral backbone) and SB insertion sites were mapped by a pooled strategy utilizing linear amplification mediated PCR (LAM-PCR), followed by Illumina next generation sequencing of the product pool.

2014-07-25 | E-GEOD-59720 | biostudies-arrayexpress

Comparative expression profiling identifies differential roles for Myogenin and p38M-NM-1 MAPK signaling in myogenesis

Project description:Mitogen activated protein kinase (MAPK) signaling regulates differentiation of many cell types. During myogenesis in particular, p38a MAPK (MAPK14) phosphorylates multiple transcriptional regulators to modulate muscle-specific gene expression. Among the p38a MAPK modulated genes is the muscle-specific transcriptional regulator Myogenin (Myog) that is also essential to complete the muscle differentiation program, and while it is known that both p38a MAPK and Myog are critically required for myogenesis, the individual contribution of each of these proteins is poorly defined. Here we show that Myog expression (in the absence of p38a MAPK signaling) is sufficient to establish expression of many late markers of muscle differentiation and to mediate cell migration. However, Myog expression alone did not led to the formation of multinucleated muscle cells, highlighting a critical role for p38a MAPK in myoblast fusion. Using comparative microarray analysis we identified p38a MAPK-dependent genes that are not regulated by Myog We generated a stable C2C12-derived cell line (C2i-Myog) that expresses a Doxycycline (Dox)-inducible cDNA encoding Flag-tagged Myog. In this system, the chemical induction of exogenous Myog (Dox) combined with the pharmacological inhibition of p38a/b MAPK signaling by SB203580 (SB) would allow us to assess the functional contribution of these two pathways during myogenesis

2012-08-01 | E-GEOD-25763 | biostudies-arrayexpress

Genome-wide expression profile of the Tet-On HCT116 inducible cell line that express either the human HNF4α2 or HNF4α8 under control of Doxycycline (DOX) [RNAseq]

Project description:Purpose: Aim of the study is to identify functional differences between the P1 and P2-HNF4α isoforms. To do this, we generated Tet-On inducible lines that express either the human (P1) HNF4α2 or (P2) HNF4α8 under control of DOX in the HCT116 human colon cancer cells. Methods: HNF4α2 and Parental lines were induced with 0.3 μg/mL DOX, while HNF4α8 line was induced with either 0.1 or 0.3 μg/mL DOX for 24 hours. Samples were generated by deep sequencing, using the Illumina TruSeq RNA. Result: There were common and unique dysregulated genes identified in the HNF4α2 and HNF4α8 lines (+DOX); more upregulated genes than downregulated genes in both the lines. Conclusion: The functional difference between HNF4α2 and HNF4α8 is that the latter tends to upregulate genes involved in proliferation and anti-apoptosis while HNF4α2 upregulates genes involved in growth suppression and cell death. Tet-On inducible HCT116 cell (Parental, HNF4α2, and HNF4α8) lines, treated with (0.0, 0.1, or 0.3 μg/mL) DOX for 24 hours, were 50bp pair-ended sequenced in triplicate using Illumina TruSeq RNA Sample Prep v2 Kit.

2015-08-28 | E-GEOD-62889 | biostudies-arrayexpress

HNF4α and TCF4 (TCF7L2) ChIPseq in Tet-On HCT116 inducible cell lines that express either the human HNF4α2 or HNF4α8 under the control of doxycycline (DOX) [ChIP-Seq]

Project description:Purpose: Aim of the study is to determine how many of the dysregulated genes in the RNAseq are direct targets of (P1) HNF4α2 and (P2) HNF4α8 and examine HNF4α and TCF4 binding in vivo. We performed ChIPseq on TCF4 in the absense or presence of DOX in the Tet-On inducible HCT116 HNF4α2 and HNF4α8 lines, and ChIPseq for HNF4α (a445 Ab) in the presence of DOX. Methods: HNF4α2 and HNF4α8 lines were induced with 0.3 μg/mL DOX for 24 hours. Samples were generated by deep sequencing, using the NEXTflex ChIPseq. Result: There were more HNF4α2 peaks than HNF4α8 peaks, with some common peaks bound by HNF4α2 and HNF4α8. Binding patterns were observed between HNF4α and TCF4. Conclusion: HNF4α2 can displace TCF4 better than HNF4α8 on AP-1 bound sites. Tet-On inducible HCT116 cell (HNF4α2 and HNF4α8) lines, treated with (0.3 μg/mL) or without DOX for 24 hours, were 50bp single-end sequenced using Illumina-compatible-NEXTflex ChIP kit (Bioo Scientific).

2015-08-28 | E-GEOD-62890 | biostudies-arrayexpress

Gene expression profiles of MCF7 with CARM1 knocked down

Project description:The goal of this study is to identify ERalpha-target genes affected by knocking down of the histone arginine methyltransferase CARM1 in MCF7 breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 knockingdown MCF7 cell line where CARM1 is decreased to 20% of endogeneous level to determine the created a Dox-inducible CARM1shRNA overexpressing MCF7 cells for evaluation of the global effects of CARM1 on ERalpha-target gene expression. MCF7-tet-on-CARM1shRNA clone 1 were treated under 4 conditions: DMSO; Dox; E2 (10nM); Dox+E2. In Dox+E2 condition, cells were pre-treated with Dox for 5 days before treating with E2 for 4 hours. 3 biological replicates were included and total of 12 samples were analyzed.

2011-06-01 | E-GEOD-26259 | biostudies-arrayexpress

Transcriptional profiling by array of stable HeLa cell line with doxycycline-inducible transcription factor E2F7 transgene

Project description:stable dox-inducible HeLa lines expressing E2F7

2012-08-02 | E-TABM-1212 | biostudies-arrayexpress

Gene expression profiles of CARM1 overexpression in MCF7

Project description:The goal of this study is to identify ERalpha-target genes affected by overexpression of the histone arginine methyltransferase CARM1 in breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 overexpressing MCF7 cell line where CARM1 is overexpressed by 2 fold to determine the created a Dox-inducible CARM1 overexpressing MCF7 cells for evaluation of the global effects of CARM1 on Eralpha-target gene expression. MCF7-tet-on-CARM1 clone 13 were treated under 4 conditions: DMSO; Dox; E2 (10nM); Dox+E2. In Dox+E2 condition, cells were pre-treated with Dox for 5 days before treating with E2 for 4 hours. 3 biological replicates were included and total of 12 samples were analyzed.

2011-06-01 | E-GEOD-26454 | biostudies-arrayexpress

Graded Nodal/Activin Signaling Governs ES Cell Fate Decisions via Differential Recruitment of Phospho-Smad2 to Oct4 and Distinct Target Gene Subsets.

Project description:The Nodal/Activin morphogens are secreted signaling molecules that form concentration gradients during early embryogenesis providing stem cells with positional information and differentiation instructions important for embryonic patterning. The molecular basis driving stem cell interpretation of signaling gradients and the undertaking of distinct cell fate decisions remains poorly understood. We show that perturbation of endogenous Nodal/Activin signaling in ES cells leads to exit from self renewal towards mesendodermal differentiation at high signaling and trophectoderm induction during low signaling. ChIP-seq of Phospho-Smad2, the downstream transcription factor of the Nodal/Activin pathway reveals binding to distinct subsets of target genes in a dose dependent manner including the promoter region of the Oct4 master regulator of stemness. Consequently, both Oct4 mRNA and protein levels are directly driven by graded Nodal/Activin signaling. Hence stem cells interpret and carry out differential Nodal/Activin signaling instructions via a corresponding gradient of Smad2 phosphorylation that selectively titers self renewal against alternative differentiation programs. 3 pSmad2 ChIP samples corresponding to ES cells pretreated for 6 hours in 10uM SB followed by 18 hours in 25ng/ml Activin, 1/5000 DMSO and 10uM SB in 20% KSR media. Controls include the corresponding input DNA for each treatment.

2011-01-31 | E-GEOD-23581 | biostudies-arrayexpress

Microarray analysis of EpiSCs undergoing reprogramming by Esrrb.

Project description:To characterize the reprogramming of epiblast stem cells (EpiSCs) into embryonic stem cells (ESCs) induced by Esrrb, we performed microarray analysis of Tet-on Esrrb EpiSCs after treatment with doxycycline (Dox).

2018-06-01 | E-MTAB-5341 | biostudies-arrayexpress

Generation and Characterization of a Conditional Ku70 Knockout Cell Line

Project description:In this study we characterize and investigate the effect of the loss of Ku70 protein in a conditional Ku70 knockout TREx-293 cell system. Loss of Ku70 protein levels was directly correlated with a loss of cell viability, supporting the observation that Ku performs an essential role in human cells. Interestingly, critical loss of average telomere length was not observed in Ku70 knockouts generated. Global quantitative proteomic analysis of whole cell extracts from Ku70 knockouts following depletion of Ku70 may indicate that Ku’s essential role in humans is not at telomeres, but a non-canonical role which is not yet fully understood.

2023-07-27 | PXD036297 | Pride

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