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ChIP of transcription factor Etv4 (Pea3) Gabpa, Histone deacetylase HDAC2, Ep300 and Histone tails H3K4me1 and H3K27ac in E11.5 limb derived cell line (14Fp cell line)

ABSTRACT: ChIP of transcription factor Etv4 (Pea3) Gabpa, Histone deacetylase HDAC2, Ep300 and Histone tails H3K4me1 and H3K27ac in E11.5 limb derived cell line (14Fp cell line)

PROVIDER: PRJNA412039 | ENA |

REPOSITORIES: ENA

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ChIP of transcription factor Etv4 (Pea3) Gabpa, Histone deacetylase HDAC2, Ep300 and Histone tails H3K4me1 and H3K27ac in E11.5 limb derived cell line (14Fp cell line)

Project description:ChIP profiling of transcription factor Etv4 (Pea3) Gabpa, Histone deacetylase HDAC2, Ep300 and Histone tails H3K4me1 and H3K27ac in E11.5 limb derived cell line (14Fp ) across the ZRS and a selection of limb development genes

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Chip-chip from Mouse E11.5 distal limb tissue cells for Gabpa, Ets1, Elf1, Etv4, Etv5 antibody

Project description:Two different groups of Ets transcription factors differentially act directly at the ZRS to define the spatial expression of Shh in the limb. Chromatin immunoprecipitation (ChIP) of Gabpa, Ets1, Etv4, Etv5 and Elf1 and by ChIP-on-chip analysis demonstrated that with the exception of Elf1 all bind directly to the Shh limb enhancer, the ZRS. Array design includes 2 biological replicates for Gabpa and Elf1, and two biological replicates and one dye swap replicate for Ets1, Etv4 and Etv5 samples.

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shRNA-mediated knockdown of ETV4 and MED25 in the prostate cell line PC3 reveals set of genes potentially coregulated by MED25 and ETV4

Project description:Our in vitro binding studies support a model whereby MED25 exhibits multivalent interactions with a subset of related ETS factors, ETV1/4/5. We hypothesize that the interaction would allow for coregulation of genes by ETV1/4/5 and MED25, acting perhaps to link the ETVs to the Mediator complex. To explore this possibility, we compared the genome occupancy for FLAG-tagged MED25 and ETV4 in the prostate cancer cell line PC3, which overexpresses ETV4. We also tested for relevance of MED25 and ETV4 binding to for gene expression in PC3s. We found a high degree of overlap in the FLAG-MED25 and ETV4 ChIPs datasets consistent with our model, and also identified a subset of target genes co-dependent on Med25 and ETV4.

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Project description:Study of differences in gene expression profiles in the mammary glands tumours of PEA3-null and wild-type PEA3 mice induced by the Her2/Neu transgene. Keywords: other

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Chip-chip from Mouse E11.5 distal limb tissue cells for Gabpa, Ets1, Elf1, Etv4, Etv5 antibody

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Target genes associated to siRNA mediated repression of Pea3 and Erm transcription factors in mammary cancerous cells

Project description:Pea3 and Erm are transcription factors belonging to the ETS family which are involved in tumorigenesis, particularly mammary oncogenesis. To elucidate the mechanism of Pea3/Erm induced tumorigenesis in mouse mammary cancerous MMT cells (ATCC CCL-51), we have down-regulated Pea3 or Erm expression in this cell line by using small interfering RNA and performed a microarray analysis using Applied Biosystems AB1700 technology to define target associated genes. Keywords: Comparative transcriptome hybridization, small interfering RNA, mouse mammary cancerous cells

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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.

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