E-MEXP-548
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-548 | ExpressionAtlas | 2025-01-22
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MEXP-548-analysis-methods.tsv | Tabular | |||
| E-MEXP-548-atlasExperimentSummary.Rdata | Rdata | |||
| E-MEXP-548-configuration.xml | Xml | |||
| E-MEXP-548-percentile-ranks.tsv | Tabular | |||
| E-MEXP-548.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 82 |
Similar Datasets
Project description:Small RNA analysis of ADAR1-knock down HeLa cells by RNAi
| PRJNA184835 | ENA
Project description:Small RNA profiles following TUT knock-down in HeLa
| PRJNA151961 | ENA
Project description:The goal of the ChIP-seq study was to investigate the distribution of the TATA-binding protein (TBP) across the human genome. TBP is the DNA-binding subunit of the basal transcription factor TFIID for RNA polymerase II (pol II) and it also participates in other complexes for the other RNA polymerase. The BTAF1 ATPase forms a stable complex with TBP and regulates its activity in pol II transcription. BTAF1 is believed to mobilize TBP from promoter and non-promoter sites. To test this hypothesis, TBP ChIP samples were prepared from human HeLa cervix carcinoma cells after knock-down of BTAF1 expression and compared to HeLa cells with a control knock-down of GAPDH. GAPDH is a cytosolic enzyme that participates in glycolysis, and its inactivation is not expected to affect the genomic distribution of TBP, and acts as negative control. ChIP samples were sequenced using SOLiD technology along with the INPUT sample to normalize the distribution of background signals within each of the two chromatin samples.
2010-03-02 | GSE17937 | GEO
Project description:Post-transcriptional gene regulation relies on hundreds of RNA binding proteins (RBPs) but the function of most RBPs is unknown. The human RBP HuR/ELAVL1 is a conserved mRNA stability regulator. We used PAR-CLIP, a method based on RNA-protein crosslinking, to identify transcriptome wide ~26,000 HuR binding sites. These sites were on average highly conserved, enriched for HuR binding motifs and mainly located in 3' untranslated regions. Surprisingly, many sites were intronic, implicating HuR in splicing. Upon HuR knock down, mRNA levels and protein synthesis of thousands of target genes was down regulated, validating functionality. HuR and miRNA binding sites tended to reside nearby but generally did not overlap. Additionally, HuR knock down triggered strong and specific up regulation of miR-7. In summary, we identified thousands of direct and functional HuR targets, found a human miRNA controlled by HuR, and propose a role for HuR in splicing. PolyA mRNA was extracted from anti HuR siRNA treated and mock transfected HeLa cells to identify changes in mRNA expression and splicing. 2x100 paired end sequencing was performed according to the protocol on the Illumina HiSeq. PARCLIP was performed as in Hafner et. Al 2010 but with an antibody against endogenous HuR (3A2, Santa Cruz, sc-5261) in unstressed HeLa cells. We used, independently, 4-thiouridine (4SU) and 6-thioguanosine (6SG) to assess a possible nucleotide bias. As our proteomics measurements required labeling of cells in a special medium we also performed PAR-CLIP on cells grown in SILAC medium. Altogether we performed three PAR-CLIP experiments: 4SU labeling in standard DMEM medium, 4SU labeling in SILAC medium (as a replicate) and 6SG labeling in SILAC medium. Small RNA was extracted from anti HuR siRNA treated and mock transfected HeLa cells to identify changes in mRNA expression. Sequencing was performed on Illumina GAII using the standard sRNA 36cycle protocol.
2011-06-29 | E-GEOD-29943 | biostudies-arrayexpress
Project description:Ars2 is a component of the nuclear cap-binding complex that is required for cellular proliferation and contributes to microRNA biogenesis. Arrays were performed to determine the repertoire of genes that change following knock-down of Ars2. Knock-down of DGCR8 was also performed to determine which changes in Ars2 knock-down cells resulted from defects in microRNA expression. 9 samples were analyzed including: three biological replicates of control siRNA-transfected HeLa cells, HeLa cells transfected with three independent siRNAs targeting Ars2, or HeLa cells transfected with three independent siRNAs targeting DGCR8.
2012-02-01 | E-GEOD-34679 | biostudies-arrayexpress
Project description:We knock down MYCN in human neuroblastoma cell line by RNAi. MYCN knock-down caused global epigenome change, including nucleosome gain on key DNA-repair genes and promoter H3K9ac down regulation.
2019-06-30 | GSE120858 | GEO
Project description:We knock down MYCN in human neuroblastoma cell line by RNAi. MYCN knock-down caused global epigenome change, including nucleosome gain on key DNA-repair genes and promoter H3K9ac down regulation.
2019-06-30 | GSE120857 | GEO
Project description:We knock down MYCN in human neuroblastoma cell line by RNAi. MYCN knock-down caused global epigenome change, including nucleosome gain on key DNA-repair genes and promoter H3K9ac down regulation.
2019-06-30 | GSE120856 | GEO
Project description:Despite the established role of the transcription factor MYC in cancer, little is known about the impact of a new class of transcriptional regulators, the long non-coding RNAs (lncRNAs), on the way MYC is able to influence cellular transcriptome. To this aim we have intersected RNA-sequencing data from two MYC-inducible cell lines and from a cohort of 91 mature B-cell lymphomas carrying, or not carrying, genetic variants resulting in MYC over-expression. By this approach, we identified 13 lncRNAs differentially expressed in IG-MYC-positive Burkitt lymphoma and regulated in the same direction by MYC in the model cell lines. Among them we focused on a lncRNA that we named MINCR, for MYC-Induced long Non-Coding RNA, showing a strong correlation with MYC expression in MYC-positive lymphomas and also in pancreatic ductal adenocarcinomas. To understand its cellular role we performed RNA interference (RNAi) experiments and found that MINCR knock-down is associated with a reduction in cellular viability, due to an impairment in cell cycle progression. Differential gene expression analysis following RNAi showed a strongly significant enrichment of cell cycle genes among the genes down-regulate following MINCR knock-down. Interestingly these genes are enriched in MYC binding sites in their promoters, suggesting that MINCR acts as a modulator of MYC transcriptional program. Accordingly, following MINCR knock-down, we observed a reduction in the binding of MYC to the promoters of selected cell cycle genes. Finally we provide evidences that down-regulation of AURKA, AURKB and CTD1 may explain the reduction in cellular proliferation observed upon MINCR knock-down. We therefore suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.
| EGAD00001001441 | EGA
Project description:Effect of PAAF1 and Spt6 knock-down on gene expression. Total RNAs were extracted from HeLa-LTR-Luc cells in which PAAF1 or Spt6 had been knock down by a specific siRNA or HeLa-LTR-Luc cells that had been transfected with a control siRNA (“si Neg”). Differentially expressed genes in PAAF1 knock-down cells were identified by microarray.
2012-05-29 | GSE32033 | GEO