Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1037166 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26729785_1.fastq.gz | Fastqsanger.gz | |||
| SRR26729785_2.fastq.gz | Fastqsanger.gz | |||
| SRR26729786_1.fastq.gz | Fastqsanger.gz | |||
| SRR26729786_2.fastq.gz | Fastqsanger.gz | |||
| SRR26729787_1.fastq.gz | Fastqsanger.gz |
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Project description:Response of HEK293-cells after transfection with EWS-FLI1. HEK293 cells were transfected with the expression vector pIRES2-EGFP containing type I EWS-FLI1 or empty control vector. For transient transfection standard DEAE dextran method was used and RNA was isolated 48h post transfection. For stable transfection cells were transfected using FuGENE 6 (Roche, Mannheim, Germany) and cells were selected with 400 ug/mL G418. DNA-microarray analysis was performed using Affymetrix HG-U133A microarrays.(see Staege et al. Cancer Res. 2004) Keywords = HEK293 Keywords = EWS-FLI1 Keywords = Ewing family tumors Keywords: other
2004-10-07 | GSE1822 | GEO
Project description:Purpose: Quantitative RT-PCR and ChIP analyses identified MAX as a transcriptional repressor of circadian BMAL1 target genes. The goal of this study is to compare the transcriptional effect of a knockdown of either MAX and BMAL1 in a human cell line (MDA-MB-231) Methods: Polyadenylated mRNA profiles of human breast cancer MDA-MB-231 cells with knocked down MAX or BMAL1 were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000 sequencer. Cells transfected with a non-targeting siRNA sequence were used as a control. RNA sequencing counts were used to determine differentially expressed genes with DeSeq2 package included in the Galaxy web platform (usergalaxy.org). Differentially expressed genes (DEGs) were defined adopting an adjust P < 0.001 as a statistical cut-off value. Results: Transcript assembly and quantification of RNA-sequencing reads identified 4863 and 4247 differentially expressed genes (DEGs) upon knockdown of BMAL1 or MAX, respectively. The comparison of the two set of genes revealed that 2391 of siBMAL1 DEGs (almost 50%) were also differentially expressed in MAX-silenced cells. Heat map and clustering analysis of this sub-set of genes revealed that more than 90% (2241 out of 2391) were coherently altered in both conditions (i.e. their expression was altered in the same direction). Consistent with our quantitative RT-PCR experiments, genes belonging to the circadian rhythm signalling were altered by both MAX and BMAL1 silencing. Conclusion: This study indicate that MAX is a part of the molecular clock transcriptional network.
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Project description:RNA-Seq analysis of MCV-miR-M1 mimic-transfected HEK293 cells
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Project description:Purpose: To identify the effect of EBV EBNA2 on cellular mRNA alternative splicings Methods: HEK293 cells were transfected with either GFP-EBV EBNA2 vector or empty vector (NC) for 48 hours. Then the cell RNA was sequenced by the Illumina NovaSeq 6000 high-throughput sequencing (RNA-seq, the second generation sequencing); and by the PacBio Sequel II platform (SMRT-seq, the third generation sequencing). Results: Log-fold changes of up- or down-regulated mRNAs between the control and experiment group were selected with a significance threshold of p<0.05. Conclusions: Our study describes the mRNA changes (including mRNA expression and mRNA alternative splicing) induced by EBV-EBNA2 in HEK293 cells
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Project description:Transcriptional profiling of human embryo kidney cells comparing control HEK293 transfected with empty vectors cells with HEK293 cells transfected with pcDNA3-ZNF191 (or ZNF191 siRNA vector). We searched for early ZNF191 target genes by using a transient overexpression and knockdown strategy in the human embryo kidney (HEK293) cells. A table of gene targets of transcription factor ZNF191 commonly identified by both strategies is appended below as a supplementary file.
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Project description:RNAseq profiling of Aire and Ctr-transfected HEK293 cells
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Project description:The MYC axis is commonly disrupted in cancer, mostly by activation of the MYC family of oncogenes, but also by genetic inactivation of MAX, the obligate partner of MYC, and of the MAX partner, MGA, both of which are members of the polycomb repressive complex, ncPRC1.6. While the oncogenic properties of the MYC family have been extensively studied, the tumor suppressor functions of MAX and MGA and the role of the MYC genes in MAX-mutant cells remain unclear. To address these knowledge gaps, we used chromatin immunoprecipitation, RNA-sequencing and mass spectrometry-based proteomic analysis in MAX-restituted and MYC oncogenic-transformed cell lines derived from human small cell lung cancer (SCLC), which is a high-grade neuroendocrine type of lung cancer. We found that MAX-mutant SCLC cells express ASCL1 and ASCL1-dependent targets, implying that these cells belong to the ASCL1-dependent group of SCLCs. In the absence of MAX, even after ectopic overexpression of MYC, we found no recruitment of MYC to the DNA. Furthermore, MAX reconstitution triggered pro-differentiation expression profiles that shifted when MAX and oncogenic MYC were co-expressed. Although ncPRC1.6 could be formed, the lack of MAX restricted global MGA occupancy, selectively driving its recruitment towards E2F6 motifs. Conversely, MAX restitution enhanced MGA occupancy and global gene repression of genes involved in different functions, including stem-cell and DNA repair/replication. Our data reveal that MAX-mutant SCLCs have ASCL1 characteristics, and are MYC-independent, and that their oncogenic features include deficient ncPRC1.6-mediated gene repression.
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Project description:PRDM9 is a histone methyltransferase expressed in meiotic germ cells that determines the location of genetic recombination hotspots through binding of its allele-specific DNA binding domain. Here we characterize the genome-wide chromatin modification for two human PRDM9 alleles (A and C) in human cell lines. HEK293 cells were transfected with both alleles and an empty vector control. Resulting chromatin was subjected to H3K4me3 ChIP followed by high-throughput sequencing. We find that different PRDM9 allele largely modified chromatin in entirely different genomic regions in somatic cells determined by the protein's zinc-finger DNA binding domains. Many of the allele-specific peaks overlap sites of meiotic double-strand breaks found in vivo in human germ cells suggesting that transient expression of PRDM9 in somatic cells can reflect binding in vivo. Identify PRDM9-dependent H3K4me3 sites by comparing modified chromatin after expression of different human PRDM9 alleles in HEK293 cells.
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