Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (expression)

ABSTRACT: Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe expression profile of peritoneal macrophages from wild-type mice pre-administrated with TLR ligands or from ATF7 knockout mice. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory.

ORGANISM(S): Mus musculus

PROVIDER: GSE71111 | GEO | 2015/08/31

SECONDARY ACCESSION(S): PRJNA290369

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (expression)

Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe expression profile of peritoneal macrophages from wild-type mice pre-administrated with TLR ligands or from ATF7 knockout mice. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory. This series contains seven sets of exression array data. For all sample, we use four CEL files generated by four biological-independent experiments.

2015-08-31 | E-GEOD-71111 | biostudies-arrayexpress

ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (ChIP)

Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe 3,811 ATF7 binding sites in mouse peritoneal macrophages, and 95% of the ATF7 signals in wild-type macrophages are lost in ATF7 knockout macrophages. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory. This series contains one set of whole genome ChIP-chip data and 2 sets of promoter array ChIP-chip data. For all sample, we use three IP .CEL files and three WCE .CEL files (they are triplicated experiments) to make one profile.

2015-08-31 | E-GEOD-71112 | biostudies-arrayexpress

ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (ChIP)

Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe 3,811 ATF7 binding sites in mouse peritoneal macrophages, and 95% of the ATF7 signals in wild-type macrophages are lost in ATF7 knockout macrophages. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory.

2015-08-31 | GSE71112 | GEO

ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory

Project description:ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory

| PRJNA290367 | ENA

The Transcription Factor ATF7 Controls Adipocyte Differentiation and Thermogenic Gene Programming.

Project description:The adipocytes functions as a central organ in the regulation of metabolic homeostasis. Factors which contribute to the adipocyte differentiation and function would be the promising targets to combat the obesity and associated metabolic disorders. The activating transcription factor 7 (ATF7), a stress-responsive chromatin regulator, has recently been shown to be involved in the energy metabolism; however, the underlying mechanisms are still unknown. Here, we show that ATF7 is required for adipocyte differentiation and it interacts with histone dimethyltransferase G9a in adipocyte to repress the interferon-stimulated genes (ISGs) expression, which suppresses adipogenesis. Ablation of ATF7 promotes the beige biogenesis and browning of inguinal white adipose tissue (iWAT). ATF7 binds to the transcription regulatory regions of Ucp1 gene, and silences it by maintaining the histone H3K9 dimethylation level. These results establish the multifunction of ATF7 in adipocyte and provide molecular insights into the epigenetic control of development and function of adipose tissues.

2018-11-09 | GSE122346 | GEO

The Transcription Factor ATF7 Controls Adipocyte Differentiation and Thermogenic Gene Programming

2018-11-10 | GSE122374 | GEO

Mus musculus

Project description:ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (expression)

| PRJNA290369 | ENA

Mus musculus

Project description:ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (ChIP)

| PRJNA290368 | ENA

Genome-wide mapping of ATF7 in total testicular germ cells

Project description:Increasing evidence indicates that paternal dietary conditions influence the metabolic disorders of offspring. Previous studies suggested the involvement of epigenetic regulation for such phenomena, but the mechanism remains elusive. To reveal the molecular function of stress-dependent epigenetic regulator ATF7 in paternal inheritance of dietry effect on offpring phenotype, we analyzed ATF7-binding profiles in testicular germ cells by ChIP-seq, DNA methylation profiles in sperm by TGBS, small RNA expression profiles in HRCS by RNA-seq,and whole expression profiles in offspring liver by expression array analysis, using wild-type and ATF7 heterozygous mutant mice fed with control diet or low-protein diet.

2020-03-09 | GSE123252 | GEO

IRF2BP2 counteracts the ATF7/JDP2 heterodimer to prevent inflammatory overactivation in AML cells

Project description:Acute myeloid leukemia (AML) is a hematological malignancy characterized by the abnormal proliferation and accumulation of immature myeloid cells in the bone marrow. Inflammation plays a crucial role in AML progression, but excessive activation of inflammatory pathways can also trigger cell death. IRF2BP2 is a chromatin regulator that has been implicated in AML pathogenesis, although its precise role in this disease is not fully understood. In this study, we demonstrate that in AML cells IRF2BP2 interacts with the transcriptional heterodimer ATF7/JDP2, which is involved to activate inflammatory pathways in AML cells. We show that IRF2BP2 is recruited by the ATF7/JDP2 dimer to chromatin and counteracts its gene activating function. Loss of IRF2BP2 leads to the overactivation of inflammatory pathways, resulting in immediate cell death. Our findings suggest that a delicate balance of activating and repressive transcriptional mechanisms establishes a pro-oncogenic inflammatory set-up in AML cells, and that manipulation of the ATF7/JDP2-IRF2BP2 regulatory axis may offer a potential vulnerability for AML treatment. Thus, our study provides new insights into the molecular mechanisms underlying AML pathogenesis and identifies a potential therapeutic target for AML treatment.

2024-05-16 | PXD041817 | Pride

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