Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

31 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling by array of mouse M1 cells expressing Batf targeting siRNA or control siRNA and treated with leukemia inhibitory factor to identify putative downstream targets of Batf

ABSTRACT: In order to identify putative downstream targets of Batf in M1 cells, a microarray analysis was performed. Briefly, M1/Neg-RNAi (expressing control siRNA with no mammalian target) and M1/Batf-RNAi cells (expressing Batf targeting siRNA) were seeded in M1 growth medium at a density of 3 X 105/ml in 100mm culture dishes. Six plates were plated for each cell type. Within each group, three were labeled as + LIF and treated with leukemia inhibitory factor (LIF) (5 ng/ml) for 6 hours the following day. After 6 hours, the cells were harvested from all plates individually and RNA prepared. 5 µg of total RNA from the three individual samples representing each subgroup (M1/Neg-RNAi + LIF, - LIF; M1/Batf-RNAi + LIF, - LIF) were combined into one pool of RNA. EJT001 represents sample "M1/Neg-RNAi, no LIF)"; EJT002 represents sample "M1/Neg-RNAi, with LIF)"; EJT003 represents sample "M1/Batf-RNAi, no LIF)"; EJT004 represents sample "M1/Batf-RNAi, with LIF)". The four pools of RNA were shipped to Genome Explorations, Inc. for analysis using Affymetrix GeneChip technology. The differentially regulated genes were identified both within each group (+ LIF compared to - LIF) and between 2 goups (M1/Neg-RNAi and M1/Batf-RNAi).

ORGANISM(S): Mus musculus

SUBMITTER: Juan Liao

PROVIDER: E-MEXP-2995 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Global gene-regulatory targets of FOSL1, FOSL2 and BATF in human Th17 cells [RNA-seq]

Project description:The aim of this study was to investigate the transciptional mechanisms governed by FOSL1, FOSL2 and BATF for regulation of human Th17 cell-function. FOSL factors were transiently perturbed using RNAi (KD) and over-expression (OE) strategies, whereas BATF was perturbed using RNAi only. RNA-seq was then performed to determine their global transciptional targets.

2022-04-12 | GSE174809 | GEO

BATF knockout B cells

Project description:compare wild type and Batf-/- B cells activated for 0 1 or 2 days in vitro. WT or Batf deficient B cells were activated in vitro with LPS for 1 or 2 days, or left untreated. B cells were purified by MACS and activated, harvested and prepped for affymetrix gene expression profiling.

2011-05-15 | E-GEOD-28736 | biostudies-arrayexpress

RNA-Seq analysis of MCV-miR-M1 mimic-transfected HEK293 cells

Project description:To determine transcriptomic changes in cellular targets induced by MCV-miR-M1. Briefly, HEK293 cells were transfected with either MCV-miR-M1-5p, MCV-miR-M1-3p or control mimic (Thermo Fisher Scientific) prior to RNA extraction and confirmation of MCV miRNA 5p and 3p expression via stem loop qRT-PCR. Total RNA libraries were prepared using TruSeq Stranded Total RNA Sample Prep Kit (Illumina, USA) and the TruSeq cDNA libraries were analysed via Illumina HiSeq2500 paired end 100bp.

2018-03-31 | E-MTAB-6526 | biostudies-arrayexpress

Bulk RNA sequencing of WT (Batf fl/fl) and Batf-/- (Batf fl/fl PLZFcre+) ILC3s sorted from small intestine [bulk RNA-seq]

Project description:Group 3 innate lymphoid cells (ILC3s) are crucial for the maintenance of host-microbiota homeostasis in gastrointestinal mucosal tissues. The mechanisms that maintain lineage identity of intestinal ILC3s, and ILC3s-mediated orchestration of microbiota and mucosal T cell immunity are elusive. Here, we identified BATF as a gatekeeper of ILC3s homeostasis in the gut. Depletion of BATF in ILC3s resulted in excessive interferon-γ production, dysbiosis, aberrant T cell immune responses and spontaneous inflammatory bowel disease (IBD), which was considerably ameliorated by removal of adaptive immunity or antibiotic treatment. Mechanistically, BATF directly regulates ILC3s identity by globally shapes chromatin landscape of ILC3s. BATF directly binds to the cis-regulatory elements of type 1 effector genes, restrains their chromatin accessibility and inhibits their expression. Conversely, BATF promotes chromatin accessibility of genes involved in MHCII antigen processing and presentation pathways. Collectively, our findings reveal BATF is a promising candidate to maintain ILC3s stability and coordinate ILC3s–mediated control of intestinal homeostasis.

2022-08-31 | GSE168076 | GEO

BATF knockout B cells

Project description:compare wild type and Batf-/- B cells activated for 0 1 or 2 days in vitro. WT or Batf deficient B cells were activated in vitro with LPS for 1 or 2 days, or left untreated.

2011-05-15 | GSE28736 | GEO

ChIP-Seq analysis of BATF, IRF4, the Jun proteins, and histone modifications in effector CD8+ T cells

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. This is an examination of 5 different transcription factors (TFs) with 5 different histone modifications in effector CD8+ T cells. Two of the TFs (BATF and IRF4) and the histone modifications were replicated. Appropriate control sequence files for ChIP input, IgG ChIP, and Total H3 are also included.

2014-03-02 | E-GEOD-54191 | biostudies-arrayexpress

Chromatin accessibility landscapes of WT (Rag1-/-) and BATF KO (Rag1-/-Batf-/-) ILC3s sorted from small intestine [ATAC-seq]

2022-08-31 | GSE168078 | GEO

BATF-JUN is critical for IRF4-mediated transcription in T cells

Project description:Interferon regulatory factor 4 (IRF4) is an IRF family transcription factor with critical roles in lymphoid development and in regulating the immune response. IRF4 binds DNA weakly owing to a carboxy-terminal auto-inhibitory domain, but cooperative binding with factors such as PU.1 or SPIB in B cells increases binding affinity, allowing IRF4 to regulate genes containing ETS–IRF composite elements (EICEs; 5'-GGAAnnGAAA-3'). Here we show that in mouse CD4+ T cells, where PU.1/SPIB expression is low, and in B cells, where PU.1 is well expressed, IRF4 unexpectedly can cooperate with activator protein-1 (AP1) complexes to bind to AP1–IRF4 composite (5'-TGAnTCA/GAAA-3') motifs that we denote as AP1–IRF composite elements (AICEs). Moreover, BATF–JUN family protein complexes cooperate with IRF4 in binding to AICEs in pre-activated CD4+ T cells stimulated with IL-21 and in TH17 differentiated cells. Importantly, BATF binding was diminished in Irf4-/- T cells and IRF4 binding was diminished in Batf-/- T cells, consistent with functional cooperation between these factors. Moreover, we show that AP1 and IRF complexes cooperatively promote transcription of the Il10 gene, which is expressed in TH17 cells and potently regulated by IL-21. These findings reveal that IRF4 can signal via complexes containing ETS or AP1 motifs depending on the cellular context, thus indicating new approaches for modulating IRF4-dependent transcription. Genome-wide transcription factors mapping and binding of IRF4, BATF, IRF8, STAT3, JUN etc in WT, Irf4-/- and Batf-/- mice in different cell types (B cells, CD4+ T cells and TH17 cells) cultured with or without IL-21 was conducted. RNA-Seq is conducted in mouse B cells, CD4+ T cells, TH1/TH2/TH9/TH17/Treg.

2012-09-18 | E-GEOD-39756 | biostudies-arrayexpress

Comparison of gene expression profiles of naÃ¯ve and in vitro effector CD8+ T cells from wild-type and BATF-/- mice

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. P14 TCR transgenic CD8+ T cells from wild-type or BATF-/- mice were examined either as naÃ¯ve cells or after 3 days of in vitro stimulation with antibodies to CD3 and CD28 in the presence of IL-2

2014-03-02 | E-GEOD-54215 | biostudies-arrayexpress

ChIPseq analysis of IRF4 and BATF in immune cells

Project description:Purpose: The purpose of this study is to find the binding partner of IRF4 in the context of Th17- cell differentiation. To this end, we have used ChIPseq analysis followed by de novo motif search around genome-wide binding sites to identify BATF as the binding partner for IRF4 in the context of not only Th17 cells but other immune cell types as well. Naïve T-cells isolated from the spleen of C57BL/6J mice are cultured under Th17, Th2 or Th0 polarizing conditions for 42 hrs and subject to ChIP using IRF4 and/or BATF antibodies followed by high-throughput sequencing. Bone marrow derived dendritic cells (BMDCs) were stimulated with LPS for 6hrs and similrly subjected to ChIPseq analysis with IRF4.

2012-09-13 | E-GEOD-40727 | 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