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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse RARgamma responsive genes in F9 teratocarcinoma cells

ABSTRACT: We compared the differentially expressed genes between the F9 Wt cells and F9 RAR gamma knock out cells before and after RA treatment. 3 replicates for each conditions. We also identified the RA responsive genes in the F9 Wt cells. Experiment Overall Design: F9 wt cells and F9 RAR gamma knock out cells are treated with RA (1 uM) or ethanol for 24 hours. 3 replicates for each condition.

ORGANISM(S): Mus musculus

SUBMITTER: Dan Su

PROVIDER: E-GEOD-8431 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiling elucidates a specific role for RARgamma in the retinoic acid-induced differentiation of F9 teratocarcinoma stem cells.

Su Dan D Gudas Lorraine J LJ

Biochemical pharmacology 20071122 5

The biological effects of all-trans-retinoic acid (RA), a major active metabolite of retinol, are mainly mediated through its interactions with retinoic acid receptor (RARs alpha, beta, gamma) and retinoid X receptor (RXRs alpha, beta, gamma) heterodimers. RAR/RXR heterodimers activate transcription by binding to RA-response elements (RAREs or RXREs) in the promoters of primary target genes. Murine F9 teratocarcinoma stem cells have been widely used as a model for cellular differentiation and RA ...[more]

PMID: 18164278

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Microarray screening of RARgamma responsive genes in F9 teratocarcinoma cells

Project description:We compared the differentially expressed genes between the F9 Wt cells and F9 RAR gamma knock out cells before and after RA treatment. 3 replicates for each conditions. We also identified the RA responsive genes in the F9 Wt cells. Keywords: mutant type

2007-12-18 | GSE8431 | GEO

Transcription profiling of F9 teratocarcinoma sublines characterized by the presence or absence of the RAR gamma nuclear retinoic acid receptor treated with trans retinoic acid and the novel retinoid, ST1926

Project description:Effect of all trans retinoic acid and the novel retinoid, ST1926, on the profile of gene expression in F9 teratocarcinoma sublines characterized by the presence or absence of the RAR gamma nuclear retinoic acid receptor

2005-12-31 | E-MEXP-361 | biostudies-arrayexpress

Genome wide expression analysis of Ctbp2 knock down mouse F9 cells

Project description:Using an RNA interference-based genetic screen in mouse F9 cells we identify the transcriptional corepressor CTBP2 as a coactivator critically required for retinoic acid (RA)-induced transcription. Here we perfom a whole genome transcriptome analysis in F9 cells expressing shRNA for Ctbp2 and Rxr in the absence or presence of retinoic acid (RA). A total of 2,754 genes were found to be upregulated (>2 fold) and 1518 genes were downregulated (>2 fold) in response to RA treatment in the control cells. We find that around 52% and 55% of upregulated genes are dependent on Ctbp2 and Rxr for activation respectively suggesting that Ctbp2 is a coactivator of RA signaling.

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Targeting the scaffolding role of LSD1 (KDM1A) poises acute myeloid leukemia cells for Retinoic Acid induced differentiation

Project description:The histone demethylase LSD1 is deregulated in several tumors, including leukemias, providing the rationale for the clinical use of LSD1 inhibitors. In acute promyelocytic leukemia (APL), pharmacological doses of retinoic acid (RA) induce differentiation of APL cells through degradation of the PML-RAR oncogene. APL cells are resistant to LSD1 inhibition or knock-out, but LSD1 inhibition sensitizes them to physiological doses of RA without altering the stability of PML-RAR, and extends survival of leukemic mice upon RA treatment. Non-enzymatic activities of LSD1 are essential to block differentiation of leukemic cells, while the combination of LSD1 inhibitors (or LSD1 knock-out) with low doses of RA releases a differentiation-associated gene expression program, not strictly dependent on changes in histone H3K4 methylation (known substrate of LSD1). An integrated proteomic/epigenomic/mutational analysis showed that LSD1 inhibitors alter the recruitment of LSD1-containing complexes to chromatin through inhibition of the interaction between LSD1 and GFI1, a relevant transcription factor in hematopoiesis.

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Transcript level in F9 teratocarcinoma WT and RARalpha knockout in presence and absence of all-trans retinoic acid

Project description:Retinoic acid receptors (RARs) α, β and γ are key regulators of embryonic development. Hematopoietic differentiation is regulated by RARα, and several types of leukemia show aberrant RARα activity. We demonstrate that RARα plays an important role in cellular memory and imprinting by regulating the CpG methylation status of specific promoter regions. We used microarrays to identify genes, which display differential expression in F9 RARalpha knockout (RARaKO) cells relative to F9 wt cells.

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Targeting the scaffolding role of LSD1(KDM1A) poises acute myeloid leukemia cells for Retinoic Acid induced differentiation [ChIP-seq]

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