Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-seq of ADNP and TRIM28 in the U2OS cell line (Human Bone Osteosarcoma Epithelial Cells)

ABSTRACT: In order to investigate the functions of the zinc finger transcription regulator ZMYM2 and the different types of ZMYM2 binding complex with TRIM28 or ADNP, we generated the ChIP-seq data of ADNP or TRIM28 in U2OS cells.

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Homo sapiens

SUBMITTER: Yaoyong Li

PROVIDER: E-MTAB-12292 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

ZMYM2-WT, ZMYM2-SIM2mut, and FOXO3 ChIP-seq in a U2OS stable cell line

Project description:Chromatin immuno-precipitation using anti-Flag (Sigma) or control IgG (Millipore) antibodies in a U2OS stable cell line. ZMYM2 has the synonym ZNF198. Note: paired-end sequencing libraires were created in this experiment but only the forward (R1) reads are available in this submission. The 'LIBRARY_LAYOUT' attribute is therefore set to be 'SINGLE' ather than 'PAIRED'.

2015-06-23 | E-MTAB-2701 | biostudies-arrayexpress

SUMO2 ChIP-seq in the starved U2OS cells

Project description:Chromatin immuno-precipitation using SUMO2 (Life Technologies) antibody in the starved U2OS cell line.

2023-06-01 | E-MTAB-12293 | biostudies-arrayexpress

SUMO2 ChIP-seq in U2OS cells

Project description:Chromatin immuno-precipitation using SUMO2 (Life Technologies) antibody in U2OS cell line.

2015-08-07 | E-MTAB-3084 | biostudies-arrayexpress

Histone H3K18ac ChIP-seq in U2OS cells

Project description:Chromatin immuno-precipitation using anti-H3K18ac antibodies in U2OS cells.

2016-04-27 | E-MTAB-3695 | biostudies-arrayexpress

FOXJ3 ChIP-seq in a U2OS stable cell line

Project description:Chromatin immuno-precipitation using anti-Flag (Sigma) antibodies in a U2OS stable cell line. Paired-end R1 and R2 reads are provided, but the processed (mapped) reads are from a single-end (R1 read only) mapping.

2015-12-03 | E-MTAB-3687 | biostudies-arrayexpress

SUMO2 ChIP-seq in MCF10A cells

Project description:Chromatin immuno-precipitation using SUMO2 (Life Technologies) antibody in MCF10A cell line, treated with epidermal growth factor for 30 minutes.

2019-07-16 | E-MTAB-7759 | biostudies-arrayexpress

RNA-seq of the U2OS cell line (Human Bone Osteosarcoma Epithelial Cells) treated with ZMYM2, TRIM28 or ADNP knock down against the control conditions.

Project description:In order to investigate the functions of the zinc finger transcription regulator ZMYM2 and the different types of ZMYM2 binding complex with TRIM28 or ADNP, we generated the RNA-seq data with ZMYM2, TRIM28 or ADNP siRNA in U2OS cells and the control cases with siNT in U2OS cells as well.

2023-06-01 | E-MTAB-12291 | biostudies-arrayexpress

CHD7 targets active gene enhancer elements to modulate ES cell-specific gene expression.

Project description:Gene expression changes were measured between mouse ES cells of three genotypes: WT Chd7, Heterzygous Chd7 Null, Homozygous Chd7 Null. The hypothesis being tested was that CHD7, a chromatin remodeling protein, functions as a transcriptional regulator. This experiment was performed to detect gene targets of CHD7-mediated regulation. We report the genome-wide binding profile of CHD7, the protein implicated in CHARGE syndrome, in mouse ES cells using ChIP-Seq technology. Combining these data with other genomic datasets, we discover CHD7 to colocalize with other transcription factors including Oct4, Nanog, Sox2, and p300 at gene enhancer elements to regulate ES cell specific gene expression. Chd7 wildtype, heterozygous, and homozygous ES cells derived from preimplantation embryos were grown on feeder cells and total RNA was isolated using Trizol. The ratio of ES to feeder cells was estimated at 5:1. ChIP sequencing of CHD7 and p300 in mouse ES cells

2010-06-15 | E-GEOD-22341 | biostudies-arrayexpress

Estrogen receptor β role in tumour suppression of triple negative breast cancer - ChIPseq experiment

Project description:Breast cancer (BC) is the most common cancer in women worldwide, and is classified in multiple subtypes, including the so called triple-negative BC (TNBC). This is characterized by lack of estrogen receptor alpha (ERα), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2/neu), that represent common targets for BC treatment. Their absence limits the number of therapies that may be applied for TNBC treatment, suggesting the need to identify novel therapeutic targets against this disease. Several studies reported that the beta ER subtype (ERβ) is expressed in a sizeable fraction of TNBCs where its presence correlates with improved patient outcome. We evaluated ERβ expression in TNBC tissues by immunohistochemistry using two validated antibodies, demonstrating presence of this protein in 28% of samples. To investigate, in this context, the role of this estrogen receptor in TNBC biology, ERβ-expressing cell lines, representing different TNBC subtypes, were generated. Cellular and functional assays confirmed the antiproliferative activity of ERβ in TNBCs. Interaction proteomics revealed in BC nuclei the presence of several protein complexes associated with this receptor involved in chromatin remodeling, miRNA maturation and mRNA transcription. Transcriptome analyses pointed out tumor subtype-specific signaling pathways deregulation. Interestingly, among these the cholesterol biosynthesis pathway was commonly downregulated in all cell lines tested. Global analyses of ERβ binding to the genome showed its recruitment to regulatory sites of Sterol Regulatory Element-Binding Protein 1 (SREBP1), indicating a direct regulation of this pathway by the receptor. These findings suggest that drugs targeting components of cholesterol biosynthesis pathway may be new potential therapeutic options for TNBC treatment.

2019-12-02 | E-MTAB-8056 | biostudies-arrayexpress

Mutation of ZMYM2 SIMs

Project description:The interaction between SUMO and ZMYM2 is mediated through specific motifs found in ZMYM2 that are called SIMs (SUMO interacting motifs). We found/characterised three SIMs in ZMYM2 and in vitro experiments showed that mutation in these residues prevent the interaction with SUMO. Microarray transcription profiling was done to study the effects of disrupting the multiSUMO binding activity of ZMYM2, assessing the differences in gene expression in cells expressing wild-type or SIM2 mutant version of ZMYM2.

2015-08-06 | E-MEXP-3880 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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