Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Subtype-specific regulatory network rewiring in acute myeloid leukemia [DNase-Hypersensitivity]

ABSTRACT: Subtype-specific regulatory network rewiring in acute myeloid leukemia [DNase-Hypersensitivity]

PROVIDER: PRJNA423045 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6391630.fastq.gz	Fastqsanger.gz
	SRR6391640.fastq.gz	Fastqsanger.gz
	SRR6391650.fastq.gz	Fastqsanger.gz
	SRR6391631.fastq.gz	Fastqsanger.gz
	SRR6391641.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 33

Similar Datasets

Subtype-specific regulatory network rewiring in acute myeloid leukemia [DNase-Hypersensitivity]

Project description:Acute myeloid leukemia is a heterogeneous disease which is subdivided into different categories defined by disease-causing mutations in transcription factors, epigenetic regulators and signalling molecules. How different mutant regulators establish AML-specific transcriptional networks is unclear. Here we performed a comprehensive analysis of mutation-specific sets of cis-regulatory elements driving gene expression in AML blast cells from a carefully selected group of patients with alterations in genes encoding transcription factors (RUNX1, CEBPA) and signalling molecules (FTL3-ITD, RAS, NPM1). We show that each mutant regulator establishes a specific transcriptional and signalling network unrelated to normal cells driving the expression of unique sets of genes required for AML survival.

2018-09-20 | GSE108246 | GEO

Subtype-specific regulatory network rewiring in acute myeloid leukemia

Project description:Subtype-specific regulatory network rewiring in acute myeloid leukemia

| PRJNA423094 | ENA

DNase I hypersensitivity with capture in mES cells

Project description:DNase I hypersensitivity with capture in mES cells

| PRJNA415942 | ENA

Subtype-specific regulatory network rewiring in acute myeloid leukemia [Hi-C]

Project description:Subtype-specific regulatory network rewiring in acute myeloid leukemia [Hi-C]

| PRJNA423089 | ENA

Subtype-specific regulatory network rewiring in acute myeloid leukemia [RNA-seq]

Project description:Subtype-specific regulatory network rewiring in acute myeloid leukemia [RNA-seq]

| PRJNA423049 | ENA

DNase hypersensitivity mapping (DNase-chip) using Nimblegen ENCODE arrays in a variety of human cell types

2009-11-01 | GSE18735 | GEO

DNase hypersensitivity mapping (DNase-chip) using Nimblegen ENCODE arrays in a variety of human cell types

Project description:DNase hypersensitivity using Nimblegen ENCODE arrays (DNase-chip) in primary human trachea epithelia (pHTE), normal human bronchial epithelia (NHBE), Caco2, HT29, human skin fibroblasts, primary human male epididymis. DNase hypersensitivity mapping is used to detect putative regulatory elements of the human genome. We digested chromatin from the above cell types with DNaseI using the DNase-chip protocol devised by Crawford et al. (Nat. Methods, 2006). Briefly, cells are lysed, chromatin is digested with increasing amounts of DNase I, digested ends are blunted in adequetely digested samples, ligated to biotinylated linkers, purified with streptavidin beads, amplified by LM-PCR. As control, randomly sonicated genomic DNA is used. LM-PCR material was labeled and hybridized to hg_17 ENCODE arrays at Nimblegen facility. DNaseI-digested chromatin was hybridized to Nimblegen ENCODE arrays (build hg17). Randomly sonicated genomic DNA was used as control. Three biological replicates on three arrays were performed for Caco2 cells, three replicates were done with skin fibroblasts (two digestions were pooled and hybridized to a single array [Sample: SkinFibro.sample2]), two replicates on two arrays were performed for pHTE, NHBE, and HT29, and a single experiment for primary male epididymis.

2009-10-31 | E-GEOD-18735 | biostudies-arrayexpress

Genome-wide maps of H3K4me2 and DNase I hypersensitivity sites in prostate cancer cell line LNCaP and breast cancer cell line MCF-7.

Project description:We report the high-throughput profiling of histone modification and DNase I hypersensitivity sites in prostate cancer and breaset cancer cells. We found that while AR binding is associated with nucleosome depletion, ER binding is not. We showed that a quantitative measure of DNase I hypersensitivity changes is a powerful tool in indentifying transcription factor cistromes. Examination of histone modification marked nucleosomes and Dnase I hypersensitivity in prostate cancer and breast cancer cells with and without hormone treatment.

2012-03-25 | E-GEOD-33216 | biostudies-arrayexpress

Whole genome DNAse hypersensitivity in human CD4+ T-cells

Project description:Mapping DNaseI hypersensitive (HS) sites is an accurate method of identifying the location of genetic regulatory elements, including promoters, enhancers, silencers, insulators, and locus control regions. We employed whole genome tiled array strategies to identify DNaseI HS sites within human primary CD4+ T cells. Keywords: whole genome tiling array DNAse hypersensitivity from two biologic replicates of CD4+ T-cells were hybridized to a whole-genome tiling array set (38 arrays each) and compared to the input DNA from the same samples.

2007-11-19 | E-GEOD-8486 | biostudies-arrayexpress

Subtype-specific regulatory network rewiring in acute myeloid leukemia.

Project description:Acute myeloid leukemia (AML) is a heterogeneous disease caused by a variety of alterations in transcription factors, epigenetic regulators and signaling molecules. To determine how different mutant regulators establish AML subtype-specific transcriptional networks, we performed a comprehensive global analysis of cis-regulatory element activity and interaction, transcription factor occupancy and gene expression patterns in purified leukemic blast cells. Here, we focused on specific subgroups of subjects carrying mutations in genes encoding transcription factors (RUNX1, CEBPα), signaling molecules (FTL3-ITD, RAS) and the nuclear protein NPM1). Integrated analysis of these data demonstrates that each mutant regulator establishes a specific transcriptional and signaling network unrelated to that seen in normal cells, sustaining the expression of unique sets of genes required for AML growth and maintenance.

| S-EPMC6330064 | biostudies-literature

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