Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA154905 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR351352.fastq.gz | Fastqsanger.gz | |||
| SRR351353.fastq.gz | Fastqsanger.gz | |||
| SRR351354.fastq.gz | Fastqsanger.gz | |||
| SRR351355.fastq.gz | Fastqsanger.gz | |||
| SRR351356.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 21 |
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE32348: Methylation specifies distinct estrogen-induced binding site repertoires of CBP to chromatin (mRNA) GSE32349: Methylation specifies distinct estrogen-induced binding site repertoires of CBP to chromatin (ChIP-Seq) Refer to individual Series
2011-10-06 | E-GEOD-32350 | biostudies-arrayexpress
Project description:Methylation specifies distinct estrogen-induced binding site repertoires of CBP to chromatin (mRNA)
| PRJNA154903 | ENA
Project description:Multiple signaling pathways ultimately modulate the epigenetic information embedded in the chromatin of gene promoters by recruiting epigenetic enzymes. We found that, in estrogen-regulated gene programming, the acetyltransferase CREB-binding protein (CBP) is specifically and exclusively methylated by the coactivator-associated arginine methyltransferase (CARM1) in vivo. CARM1-dependent CBP methylation and p160 coactivators were required for estrogen-induced recruitment to chromatin targets. Notably, methylation increased the histone acetyltransferase (HAT) activity of CBP and stimulated its autoacetylation. Comparative genome-wide chromatin immunoprecipitation sequencing (ChIP-seq) studies revealed a variety of patterns by which p160, CBP, and methyl-CBP (meCBP) are recruited (or not) by estrogen to chromatin targets. Moreover, significant target gene-specific variation in the recruitment of (1) the p160 RAC3 protein, (2) the fraction of a given meCBP species within the total CBP, and (3) the relative recruitment of different meCBP species suggests the existence of a target gene-specific âfingerprintâ for coregulator recruitment. Crossing ChIP-seq and transcriptomics profiles revealed the existence of meCBP âhubsâ within the network of estrogen-regulated genes. Together, our data provide evidence for an unprecedented mechanism by which CARM1-dependent CBP methylation results in gene-selective association of estrogen-recruited meCBP species with different HAT activities and specifies distinct target gene hubs, thus diversifying estrogen receptor programming. Examination of estrogen-induced binding site in H3396 cells under Estrogen (E2) or Ethanol (EtOH) treatment: CBP in E2; CBP in EtOH (two technical replicate); CBPR742m in E2 (two technical replicates); CBPR768m in E2; CBPR768m in EtOH; CBPR2151m in E2; CBPR2151m in EtOH; Estrogen receptor alpha (ERa) in E2; ERa in EtOH; Total Histone 3 and 4 acetylated in E2; H3K18ac in E2; H3K18ac in EtOH; Polymerase II (PolII) in E2; PolII in EtOH; RAC3 in E2; Input DNA sample in E2
2011-10-06 | E-GEOD-32349 | biostudies-arrayexpress
Project description:Multiple signaling pathways ultimately modulate the epigenetic information embedded in the chromatin of gene promoters by recruiting epigenetic enzymes. We found that, in estrogen-regulated gene programming, the acetyltransferase CREB-binding protein (CBP) is specifically and exclusively methylated by the coactivator-associated arginine methyltransferase (CARM1) in vivo. CARM1-dependent CBP methylation and p160 coactivators were required for estrogen-induced recruitment to chromatin targets. Notably, methylation increased the histone acetyltransferase (HAT) activity of CBP and stimulated its autoacetylation. Comparative genome-wide chromatin immunoprecipitation sequencing (ChIP-seq) studies revealed a variety of patterns by which p160, CBP, and methyl-CBP (meCBP) are recruited (or not) by estrogen to chromatin targets. Moreover, significant target gene-specific variation in the recruitment of (1) the p160 RAC3 protein, (2) the fraction of a given meCBP species within the total CBP, and (3) the relative recruitment of different meCBP species suggests the existence of a target gene-specific “fingerprint” for coregulator recruitment. Crossing ChIP-seq and transcriptomics profiles revealed the existence of meCBP “hubs” within the network of estrogen-regulated genes. Together, our data provide evidence for an unprecedented mechanism by which CARM1-dependent CBP methylation results in gene-selective association of estrogen-recruited meCBP species with different HAT activities and specifies distinct target gene hubs, thus diversifying estrogen receptor programming. Examination of estrogen-induced transcription in H3396 cells
2011-10-06 | E-GEOD-32348 | biostudies-arrayexpress
Project description:Multiple signaling pathways ultimately modulate the epigenetic information embedded in the chromatin of gene promoters by recruiting epigenetic enzymes. We found that, in estrogen-regulated gene programming, the acetyltransferase CREB-binding protein (CBP) is specifically and exclusively methylated by the coactivator-associated arginine methyltransferase (CARM1) in vivo. CARM1-dependent CBP methylation and p160 coactivators were required for estrogen-induced recruitment to chromatin targets. Notably, methylation increased the histone acetyltransferase (HAT) activity of CBP and stimulated its autoacetylation. Comparative genome-wide chromatin immunoprecipitation sequencing (ChIP-seq) studies revealed a variety of patterns by which p160, CBP, and methyl-CBP (meCBP) are recruited (or not) by estrogen to chromatin targets. Moreover, significant target gene-specific variation in the recruitment of (1) the p160 RAC3 protein, (2) the fraction of a given meCBP species within the total CBP, and (3) the relative recruitment of different meCBP species suggests the existence of a target gene-specific “fingerprint” for coregulator recruitment. Crossing ChIP-seq and transcriptomics profiles revealed the existence of meCBP “hubs” within the network of estrogen-regulated genes. Together, our data provide evidence for an unprecedented mechanism by which CARM1-dependent CBP methylation results in gene-selective association of estrogen-recruited meCBP species with different HAT activities and specifies distinct target gene hubs, thus diversifying estrogen receptor programming.
2011-10-07 | GSE32348 | GEO
Project description:Multiple signaling pathways ultimately modulate the epigenetic information embedded in the chromatin of gene promoters by recruiting epigenetic enzymes. We found that, in estrogen-regulated gene programming, the acetyltransferase CREB-binding protein (CBP) is specifically and exclusively methylated by the coactivator-associated arginine methyltransferase (CARM1) in vivo. CARM1-dependent CBP methylation and p160 coactivators were required for estrogen-induced recruitment to chromatin targets. Notably, methylation increased the histone acetyltransferase (HAT) activity of CBP and stimulated its autoacetylation. Comparative genome-wide chromatin immunoprecipitation sequencing (ChIP-seq) studies revealed a variety of patterns by which p160, CBP, and methyl-CBP (meCBP) are recruited (or not) by estrogen to chromatin targets. Moreover, significant target gene-specific variation in the recruitment of (1) the p160 RAC3 protein, (2) the fraction of a given meCBP species within the total CBP, and (3) the relative recruitment of different meCBP species suggests the existence of a target gene-specific âfingerprintâ for coregulator recruitment. Crossing ChIP-seq and transcriptomics profiles revealed the existence of meCBP âhubsâ within the network of estrogen-regulated genes. Together, our data provide evidence for an unprecedented mechanism by which CARM1-dependent CBP methylation results in gene-selective association of estrogen-recruited meCBP species with different HAT activities and specifies distinct target gene hubs, thus diversifying estrogen receptor programming.
2011-10-07 | GSE32349 | GEO
Project description:The Estrogen Receptor cofactors SRC1 (NCOA1, KAT13A), SRC2 (NCOA2, GRIP1, TIF2, KAT13C) , SRC3 (NCOA3, AIB1, KAT13B, Rac3) , CBP and p300 are assessed for their genome-wide chromatin binding capacities in the breast cancer cell line MCF7. To determine the Estrogen Receptor dependency of interactions, experiments were performed in the absence of hormone and after Estradiol treatment. In addition, the data were compared with Estrogen Receptor ChIP-seq data from the same timepoint of Estradiol treatment.
2011-10-25 | E-MTAB-785 | biostudies-arrayexpress
Project description:The Estrogen Receptor cofactors SRC1 (NCOA1, KAT13A), SRC2 (NCOA2, GRIP1, TIF2, KAT13C) , SRC3 (NCOA3, AIB1, KAT13B, Rac3) , CBP and p300 are assessed for their genome-wide chromatin binding capacities in the breast cancer cell line MCF7. To determine the Estrogen Receptor dependency of interactions, experiments were performed in the absence of hormone and after Estradiol treatment. In addition, the data were compared with Estrogen Receptor ChIP-seq data from the same timepoint of Estradiol treatment.
2011-10-25 | E-MTAB-788 | biostudies-arrayexpress
Project description:CREB-binding protein (CBP, also known as nejire) is a transcriptional co-activator that is conserved in metazoans. We have generated CBP ChIP-seq data from Drosophila S2 cells and compared it to modENCODE data. This shows that CBP is bound at genomic sites with a wide range of functions. As expected, we find that CBP is bound at active promoters and enhancers. In addition, we find that the strongest CBP sites in the genome are found at Polycomb Response Elements embedded in histone H3 lysine 27 trimethylated (H3K27me3) chromatin, where they correlate with binding of the Pho repressive complex. Interestingly, we find that CBP also binds to most insulators in the genome. At a subset of these, CBP may regulate insulating activity, measured as the ability to prevent repressive H3K27 methylation from spreading into adjacent chromatin. ChIP seq in Drosophila S2 cells using two different antibodies against CBP (nejire), one raised in rabbit against amino acids 2540-3190 (CBP rb), and one raised in guinea-pig against amino acids 1-178 (CBP gp)
2015-11-06 | E-GEOD-64464 | biostudies-arrayexpress