Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA154023 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR332351.fastq.gz | Fastqsanger.gz | |||
| SRR332352.fastq.gz | Fastqsanger.gz | |||
| SRR332353.fastq.gz | Fastqsanger.gz | |||
| SRR332354.fastq.gz | Fastqsanger.gz | |||
| SRR332355.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 17 |
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Project description:This SuperSeries is composed of the following subset Series: GSE31412: Expression changes in HeLa cells treated with siRNA against HCFC1 or control luciferase GSE31417: Genome-wide study of HCFC1 binding sites and its associated transcription factors in cycling Human HeLa cells Refer to individual Series
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Project description:Analysis of transcriptional regulation in human cells has implicated a large number of promoter-specific DNA-binding proteins that regulate transcription via diverse mechanisms. In some cases, these DNA-sequence-specific factors associate with intermediaries that orchestrate interactions with the chromatin-modifying enzymes. One such intermediary is HCF-1 (host-cell factor-1; HCFC1). HCF-1, first identified for its involvement in herpes-simplex virus transcription and subsequently shown to be an important cell-cycle regulator, has a poorly defined role in genome-wide transcriptional regulation. We show here, by chromatin immunoprecipitation followed by high-throughput sequence analysis (ChIP-seq), that HCF-1 is a major transcriptional start site associated factor, whose promoter association correlates positively with transcriptional activity. Thus, in HeLa cells HCF-1 is observed on 5400 generally active CpG-island promoters. Examination of the DNA sequences underlying the HCF-1-binding sites revealed three sequence motifs associated with the binding of (i) ZNF143 and Ronin/THAP11, (ii) GABP, and (iii) YY1 sequence-specific transcription factors. Subsequent ChIP-seq analysis of these four transcription factors revealed a large co-association of HCF-1 with these four transcription factors at approximately 90% of HCF-1-bound promoters. These studies suggest that a relatively small number of transcription factors -- some (ZNF143 and Ronin/THAP11) in novel combinations -- play a major role in HeLa-cell transcriptional regulation in association with HCF-1. This experiment includes the sequencing data of material obtained from chromatin immunoprecipitation using antibodies against HCFC1(antibodies against the C-subunit and the N-subunit), PolII(antibody against the RPB2 subunit), H3K36ME3 and H3K4Me3 histone modifications, ZNF143, THAP11, GABPalpha and YY1. It also includes control data of the Input material. All of them were done using HeLa cycling cells.
2012-07-31 | E-GEOD-31417 | biostudies-arrayexpress
Project description:Genome-wide characterization of binding sites for heat shock transcription factors HSF1 and HSF2 in freely cycling and mitotic K562 cells in optimal growth conditions and upon 30 min heat stress at 42C
2013-08-04 | GSE43579 | GEO
Project description:The exon junction complex (EJC) is a central effector of mRNAs fate, linking nuclear processing to mRNA transport, translation and surveillance. Little is known about its transcriptome-wide targets. We used high-throughput sequencing after crosslinking and immunoprecipitation (HITS-CLIP) in human cells to identify the binding sites of the DEAD-box helicase eIF4AIII, an EJC core component. CLIP reads form peaks mainly located in spliced mRNAs. Most expressed exons harbour peaks equally distributed between the canonical EJC region ∼24 nucleotides upstream of exonic junctions and other non-canonical regions. Unexpectedly, both are preferentially associated to unstructured and purine-rich sequences containing the motif GAAGA, a potential binding site of EJC-associated factors. Therefore, EJC positions vary spatially and quantitatively between exons. This transcriptome-wide mapping of human eIF4AIII reveals unanticipated aspects of the EJC and broadens its potential impact on post-transcriptional regulation. To identify direct RNA binding sites of the EJC core component eIF4AIII, two biological CLIP-seq replicates were performed in HeLa cells. Additionally, mRNA-seq of the HeLa transcriptome was performed to normalize for the mRNA expression levels.
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