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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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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

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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

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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]

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

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

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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

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

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

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