Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA150331 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR393689.fastq.gz | Fastqsanger.gz | |||
| SRR393690.fastq.gz | Fastqsanger.gz | |||
| SRR393691.fastq.gz | Fastqsanger.gz | |||
| SRR393692.fastq.gz | Fastqsanger.gz | |||
| SRR393693.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 11 |
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Project description:Using DNase-seq, mRNA-seq and publicly available ChIP-seq data sets, we examined the role of chromatin accessibility (DNase-seq) in androgen receptor binding to the genome (ChIP-seq) and AR-mediated transcriptional changes (mRNA-seq). Our data reveals genome-wide changes in chromatin structure that correspond to AR binding and differential gene expression. A focused examination of DNase-seq data around androgen receptor motifs within androgen receptor ChIP-seq peaks reveals distinct patterns of protection from DNaseI cleavage. Examination of chromatin accessibility (DNase-seq), AR binding (AR ChIP-seq), and transcription (mRNA-seq) in LNCaP cells before and after 12 hours of 1 nM R1881 treatment This Series represents the RNA-Seq data only. Exon microarray data generated under the same conditions is available through GSE15805. The DNase-seq data is publicly available through GSE32970 as well as the UCSC genome browser (genome.ucsc.edu) under Regulation::ENCODE DNase/FAIRE::Duke DNaseI HS:LNCaP and LNCaP + Andro. The accession numbers for the ChIP-seq experiments used are GSE14097 and GSE28126.
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Project description:Using DNase-seq, mRNA-seq and publicly available ChIP-seq data sets, we examined the role of chromatin accessibility (DNase-seq) in androgen receptor binding to the genome (ChIP-seq) and AR-mediated transcriptional changes (mRNA-seq). Our data reveals genome-wide changes in chromatin structure that correspond to AR binding and differential gene expression. A focused examination of DNase-seq data around androgen receptor motifs within androgen receptor ChIP-seq peaks reveals distinct patterns of protection from DNaseI cleavage.
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Project description:We investigated the composition of chromatin protein network around endogenous androgen receptor (AR) in VCaP castration resistant prostate cancer cells using recently developed chromatin-directed proteomic approach called ChIP-SICAP . The androgen-induced AR chromatin protein network contained expected TFs, e.g. HOXB13, chromatin remodeling proteins, e.g. SMARCA4, and several novel candidates not previously associated with AR, e.g. prostate cancer biomarker SIM2. Based on these findings, the role of SMARCA4 and SIM2 was further characterized at AR chromatin domains . Silencing of SIM2 altered chromatin accessibility at a similar number of AR-binding sites as SMARCA4, an established ATPase subunit of the BAF chromatin remodeling complex, often aberrantly expressed in prostate cancer. Despite the wide co-occurrence on chromatin of SMARCA4 and AR, depletion of SMARCA4 influenced chromatin accessibility and expression of a restricted set of AR target genes, in particular those involved in cell morphogenetic changes in epithelial-mesenchymal transition. Silencing of SIM2, in turn, affected the expression of a much larger group of androgen-regulated genes, e.g. those involved in cellular responses to external stimuli and steroid hormone stimulus. The silencing also reduced proliferation of VCaP cells and tumor size in chick embryo chorioallantoic membrane assay, further suggesting the importance of SIM2 in the regulation prostate cancer cells.
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