Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Integration of chromatin accessibility and gene expression data with cisREAD reveals a switch from PU.1/SPIB-driven to AP-1-driven gene regulation during B cell activation [RNA-Seq]

ABSTRACT: Integration of chromatin accessibility and gene expression data with cisREAD reveals a switch from PU.1/SPIB-driven to AP-1-driven gene regulation during B cell activation [RNA-Seq]

PROVIDER: PRJNA906585 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22446851.fastq.gz	Fastqsanger.gz
	SRR22446852.fastq.gz	Fastqsanger.gz
	SRR22446853.fastq.gz	Fastqsanger.gz
	SRR22446854.fastq.gz	Fastqsanger.gz
	SRR22446855.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 22

Similar Datasets

Integration of chromatin accessibility and gene expression data with cisREAD reveals a switch from PU.1/SPIB-driven to AP-1-driven gene regulation during B cell activation [RNA-Seq]

Project description:Human B cell differentiation into antibody secreting plasma cells is a critical process in the adaptive immune response whose regulation at the genetic level remains incompletely understood. To reveal the temporal sequence of transcription factor driven cellular changes we generated chromatin accessibility (ATAC-seq) and gene expression (RNA-seq) data from the in vitro differentiation of human B cells into plasma cells. Data was gathered from three biological replicates using a published 13-day protocol of cytokine addition to drive differentiation. Using a new computational method, cisREAD (cis-Regulatory Elements Across Differentiation), we defined a core set of cis regulatory elements that are confidently linked to the dynamic binding of transcription factors and changes in gene expression. This confirmed known aspects of the differentiation process and revealed novel understanding, including a switch from PU.1/SPIB-driven to AP-1-driven genetic regulation associated with B cell activation.

2023-09-21 | GSE219011 | GEO

Integration of chromatin accessibility and gene expression data with cisREAD reveals a switch from PU.1/SPIB-driven to AP-1-driven gene regulation during B cell activation [ATAC-Seq]

2023-09-21 | GSE219009 | GEO

Integration of chromatin accessibility and gene expression data with cisREAD reveals a switch from PU.1/SPIB-driven to AP-1-driven gene regulation during B cell activation

Project description:Integration of chromatin accessibility and gene expression data with cisREAD reveals a switch from PU.1/SPIB-driven to AP-1-driven gene regulation during B cell activation

| PRJNA906582 | ENA

Integration of chromatin accessibility and gene expression data with cisREAD reveals a switch from PU.1/SPIB-driven to AP-1-driven gene regulation during B cell activation [ATAC-Seq]

Project description:Integration of chromatin accessibility and gene expression data with cisREAD reveals a switch from PU.1/SPIB-driven to AP-1-driven gene regulation during B cell activation [ATAC-Seq]

| PRJNA906586 | ENA

SPIB and BATF provide alternate determinants of IRF4 occupancy in Diffuse Large B-cell Lymphoma linked to disease heterogeneity

Project description:ChIP-seq data for the transcription factors (TFs) IRF4, PU.1 and SPIB from the cell lines OCI-LY3, OCI-LY10 and H929, and BATF from the cell lines OCI-Ly3 and OCI-Ly10. In addition ChIP-seq for the TFs IRF4, PU.1 and SPIB from the cell line OCI-LY3 following transfections of scramble/SPIB-siRNA. ChIP-seq data for the transcription factors (TFs) IRF4, PU.1 and SPIB from the cell lines OCI-LY3, OCI-LY10 and H929, and BATF from the cell lines OCI-Ly3 and OCI-Ly10. In addition ChIP-seq for the TFs IRF4, PU.1 and SPIB from the cell line OCI-LY3 following transfections of scramble/SPIB-siRNA.

2014-06-03 | E-GEOD-56857 | biostudies-arrayexpress

The Ets-family transcription factors PU.1 and SpiB are redundantly required by mature B cells to sense and respond to environmental cues

Project description:Humoral immunity requires B cells to respond to multiple stimuli, including antigen, membrane and soluble ligands and microbial products. Ets-family transcription factors regulate many aspects of hematopoiesis, although their roles in humoral immunity have proven difficult to decipher, potentially due to redundancy between the family members. Here we show that mice lacking both PU.1 and SpiB in mature B cells are unable to respond protein antigen, preventing germinal center formation and high-affinity antibody production. Mutant B cells also showed impaired survival following engagement of the CD40 and TLR pathways, but paradoxically enhanced plasma cell differentiation. PU.1 and SpiB control the expression of many components of the BCR signaling pathway and the receptors for CD40L, BAFF and toll ligands. Thus PU.1 and SpiB function enables B cells to appropriately respond to environmental cues.

2017-09-21 | GSE90094 | GEO

SPIB and BATF provide alternate determinants of IRF4 occupancy in Diffuse Large B-cell Lymphoma linked to disease heterogeneity

2014-06-03 | GSE56857 | GEO

Integration of chromatin accessibility and gene expression data with cisREAD reveals a switch from PU.1/SPIB-driven to AP-1-driven gene regulation during B cell activation

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-21 | GSE219012 | GEO

The impact of SpiB overexpression on gene expression profile in A549 cells

Project description:SpiB, an Ets family transcription factor, is expressed exclusively in mature B cells, T-cell progenitors, and plasmacytoid dendritic cells. To understand the genes regulated by SpiB in epithelial cells, we overexpressed SpiB in lung cancer cell line A549 and examined the change of transcription profile using Agilent SurePrint G3 Human Gene Expression 8x60K v2 Microarray (Agilent Technologies).

2016-11-30 | GSE90645 | GEO

PU.1-driven gene regulation in HSPC under chronic inflammatory conditions

Project description:PU.1-driven gene regulation in HSPC under chronic inflammatory conditions

| PRJNA994150 | ENA