Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

10 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Androgen Receptor (AR) targets in a cell line from the mouse proximal caput epididymus

ABSTRACT: Sequence data represent a profile of AR network targets in proliferating and non-proliferating P17 cells without cross linking AR to DNA prior to purification. P17 cells were derived from the mouse epididymal cell line PC1 by genetic modification to express a tagged wild type mouse AR cDNA (N-TAP-mAR). N-TAP-mAR allows purification of multi-protein complexes and their genomic targets with FLAG antibody coupled magnetic beads under native conditions. comparison of AR targets in proliferating versus non-proliferating cells using the PC1 WT cell line (not expressing a tagged AR) as a negative control.

ORGANISM(S): Mus musculus

SUBMITTER: Katrin Mooslehner

PROVIDER: E-GEOD-38656 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide identification of PIF1-binding sites and direct-target genes of PIF1 transcriptional regulation in skotomorphogenesis

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF1, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF1 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Three biological replicates data of PIF1-binding sites were collected by comparing the parallel ChIP samples from Myc-epitope-tagged-PIF1 (P1M) overexpressing transgenic seedlings and the wild-type (WT) control.

2014-10-02 | E-GEOD-43283 | biostudies-arrayexpress

Genome-wide identification of PIF4-binding sites and direct-target genes of PIF4 transcriptional regulation in skotomorphogenesis

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF4, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF4 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Three biological replicates data of PIF4-binding sites were collected by comparing the parallel ChIP samples from Myc-epitope-tagged-PIF4 (P1M) overexpressing transgenic seedlings and the wild-type (WT) control.

2014-10-02 | E-GEOD-43284 | biostudies-arrayexpress

RGA binding sites in Arabidopsis thaliana seedlings

Project description:DELLA proteins act as hubs that relay environmental information to the multiple transcriptional circuits that control growth and development through physical interaction with transcription factors from different families. We have analyzed the presence of one DELLA protein at the Arabidopsis genome by chromatin immunoprecipitation coupled to large-scale sequencing and we find that it binds at the promoters of multiple genes. Enrichment analysis shows a strong preference for cis elements recognized by specific transcription factor families. In particular, we demonstrate that DELLA proteins are recruited by type-B ARABIDOPSIS RESPONSE REGULATORS (ARR) to the promoters of cytokinin-regulated genes, where they act as transcriptional co-activators. The biological relevance of this mechanism is underpinned by the necessity of simultaneous presence of DELLAs and ARRs to restrict root meristem growth and to promote photomorphogenesis. Provided are 3 biological replicates analysing RGA binding sites in Arabidopsis seedlings. ChIP-seq was performed on plants expressing RGA-GFP under the native RGA promoter and on non-transgenic control plants as reference

2015-07-23 | E-GEOD-59187 | biostudies-arrayexpress

Genome-wide identification of PIF3-binding sites and direct-target genes of PIF3 transcriptional regulation in skotomorphogenesis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-02-01 | E-GEOD-39217 | biostudies-arrayexpress

ATAC-seq of human monocytes and human monocyte-derived cells.

Project description:ATAC-seq was performed to map changes in chromatin accessibility in monocytes during in vitro differentiation. In addition to control cells, we also studied the impact of siRNA mediated knock-down of key transcription factors on accessible chromatin in monocyte-derived dendritic cells.

2021-02-03 | E-MTAB-9926 | biostudies-arrayexpress

Chromatin accessibility in human monocytes differentiation (3D-MO)

Project description:This dataset consists of ATAC-seq data from human monocytes, monocyte-derived dendritic cells or monocyte-derived macrophages as well as monocyte-derived cells that were subjected to siRNA treatment targeting CTCF or RAD21. In total, it includes 39 samples.

2022-06-24 | E-MTAB-10846 | biostudies-arrayexpress

Genome-wide identification of PIF3-binding sites and direct-target genes of PIF3 transcriptional regulation in skotomorphogenesis [ChIP-Seq]

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF1, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF3 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Four biological replicates data of PIF3-binding sites were collected by comparing the parallel ChIP samples from transgenic seedlings overexpressing Myc-epitope-tagged PIF3 (35S:PIF3-5xMyc, P3M) in pif3-3 null mutant background and the wild-type (WT) control.

2013-02-01 | E-GEOD-39215 | biostudies-arrayexpress

FoxA1 inhibits androgen receptor expression and suppresses prostate cancer metastasis [LNCaP, ChIP-seq]

Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated LNCaP cells with stable FoxA1 knockdown. We performed AR/FoxA1 ChIP-seq and microarray analysis of these cells. ChIP_Seq examination of AR and FoxA1 binding sites in LNCaP shCtrl and shFoxA1 cells

2014-06-02 | E-GEOD-37345 | biostudies-arrayexpress

FoxA1 inhibits androgen receptor expression and suppresses prostate cancer metastasis [DU145, ChIP-seq]

Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. ChIP-Seq examination of AR and FoxA1 binding sites, FAIRE-seq detection of open chromatin genomic regions in DU145 AR +/- FOXA1 cells

2014-06-02 | E-GEOD-47987 | biostudies-arrayexpress

Genome-wide mapping of FOXM1 binding reveals co-binding with oestrogen receptor alpha in breast cancer cells (ChIP-seq)

Project description:The forkhead transcription factor FOXM1 is a key regulator of the cell cycle and is overexpressed in cancer. Increased levels of FOXM1 are associated with both poor prognosis and oestrogen receptor (ERalpha) status in primary breast cancer. In this study, we map FOXM1 binding genome wide in both ERalpha-positive (MCF-7) and -negative (MDA-MB-231) breast cancer cells. We identify a common set of FOXM1 binding events at cell cycle-regulating genes, but in addition, in MCF-7 cells we find a high level of concordance with ERalpha-binding regions. FOXM1 binding at these co-binding sites is dependent on ERalpha binding, as depletion of ER protein levels reduced FOXM1 binding. FOXM1 interacts directly with both ERalpha co-activator CARM1 and is required for H3 arginine methylation at the ERalpha complex. Inhibition of FOXM1 activity with the ligand thiostrepton resulted in decreased FOXM1 binding at cca. 1400 sites genome wide and reduced expression of genes correlated with poor prognosis in ERalpha-positive tumour samples. These data demonstrate a novel role for the forkhead protein FOXM1 as an ERalpha cofactor and provide insight into the role of FOXM1 in ERalpha-positive breast cancer. The FOXM1-binding sites were mapped by ChIP-Seq in MCF-7 and MDA-MB-231 cells. Cells were treated either with thiostrepton, a FOXM1 inhibitor, or with DMSO (as control). Four replicates were performed in MCF7 cells and two replicates in MDA-MB-231 cells.

2013-01-07 | E-GEOD-40762 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data