Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq and ATAC-seq to study dendritic cell heterogeneity

ABSTRACT: RNA-seq and ATAC-seq to study dendritic cell heterogeneity

PROVIDER: PRJNA534273 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8945530_1.fastq.gz	Fastqsanger.gz
	SRR8945530_2.fastq.gz	Fastqsanger.gz
	SRR8945540_1.fastq.gz	Fastqsanger.gz
	SRR8945540_2.fastq.gz	Fastqsanger.gz
	SRR8945550_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 76

Similar Datasets

ATAC-seq of dendritic cell progenitors

Project description:ATAC-seq of dendritic cell progenitors

| PRJNA546582 | ENA

ATAC-seq of human dendritic cells

Project description:ATAC-seq of human dendritic cells

| PRJNA612317 | ENA

Histone ChIP-seq and ATAC-seq of dendritic cell progenitors

Project description:Histone ChIP-seq and ATAC-seq of dendritic cell progenitors

| PRJNA546579 | ENA

ATAC-seq of human dendritic cells

Project description:Human dendritic cells (DCs) comprise subsets with distinct phenotypic and functional characteristics, but the transcriptional programs that dictate their identity remain elusive. Here, we collected global chromatin accessibility profiles across resting and stimulated human DC subsets by means of the assay for transposase-accessible chromatin using sequencing (ATAC-seq). We uncovered chromatin accessibility specific for each subset and discovered previously undescribed transcriptional regulators of DC function. By comparing responses of plasmacytoid DCs to type I interferon -producing and -not producing conditions, we identified genetic programs related to their function. Finally, by intersecting chromatin accessibility with genome-wide association studies, we recognized DC subset-specific enrichment of heritability in autoimmune diseases. Our results unravel the basis of human DC subset heterogeneity and provide a framework for their analysis in disease pathogenesis.

2020-09-22 | GSE146896 | GEO

Restoring Tumor Immunogenicity with Dendritic Cell Reprogramming [ATAC-seq]

Project description:Restoring Tumor Immunogenicity with Dendritic Cell Reprogramming [ATAC-seq]

| PRJNA824120 | ENA

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

A negative feedback loop of transcription factors specifies alternative dendritic cell chromatin states (ATAC-Seq)

Project description:During hematopoiesis, cells originating from the same stem cell reservoir differentiate into distinct cell types. The mechanisms enabling common progenitors to differentiate into distinct cell fates are not fully understood. Here, we identify chromatin-regulating and cell-fate-determining transcription factors (TF) governing dendritic cell (DC) development by annotating the enhancer and promoter landscapes of the DC lineage. Combining these analyses with detailed over-expression, knockdown and ChIP-Seq studies, we show that Irf8 functions as a plasmacytoid DC epigenetic and fate-determining TF, regulating massive, cell-specific chromatin changes in thousands of pDC enhancers. Importantly, Irf8 forms a negative feedback loop with Cebpb, a monocyte-derived DC epigenetic fate-determining TF. We show that using this circuit logic, differential activity of TF can stably define epigenetic and transcriptional states, regardless of the microenvironment. More broadly, our study proposes a general paradigm that allows closely related cells with a similar set of signal-dependent factors to generate differential and persistent enhancer landscapes. Here we profiled accessible chromatin of moDC and pDC using ATAC-seq assay, developed by Buenrostro et al. (2013)

2014-12-14 | E-GEOD-62703 | biostudies-arrayexpress

ATAC-seq/ChIP part

Project description:Epigenetics: ATAC-seq and ChIP-seq data

| EGAS00001006520 | EGA

Subtype Heterogeneity and Epigenetic Convergence in Neuroendocrine Prostate Cancer [ATAC-seq]

Project description:Subtype Heterogeneity and Epigenetic Convergence in Neuroendocrine Prostate Cancer [ATAC-seq]

| PRJNA657289 | ENA

Chromatin accessibility (ATAC-seq) of human acute leukemias and healthy donors

Project description:ATAC-seq of 79 primary samples obtained from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). Moreover, ATAC-seq of CD34+ HSPCs from 3 healthy donors are included. ATAC-seq was performed as described (Buenrostro et al., 2013) with a modification in the lysis buffer to reduce mitochondrial DNA contamination. Due to patient confidentiality considerations, the raw data files for this dataset have been deposited to the EGA controlled-access archive under the accession numbers EGAS00001007094 (study); EGAD00001011050 (dataset).

2023-08-31 | E-MTAB-13118 | 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