Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Control of Inflammatory Response by Tissue Microenvironment [ChIP-seq]

ABSTRACT: Control of Inflammatory Response by Tissue Microenvironment [ChIP-seq]

PROVIDER: PRJNA1120921 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29313266.fastq.gz	Fastqsanger.gz
	SRR29313267.fastq.gz	Fastqsanger.gz
	SRR29313268.fastq.gz	Fastqsanger.gz
	SRR29313269.fastq.gz	Fastqsanger.gz
	SRR29313270.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 14

Similar Datasets

Control of Inflammatory Response by Tissue Microenvironment

Project description:Control of Inflammatory Response by Tissue Microenvironment

| PRJNA1124074 | ENA

Control of Inflammatory Response by Tissue Microenvironment [ChIP-Seq]

Project description:Control of Inflammatory Response by Tissue Microenvironment [ChIP-Seq]

| PRJNA1124075 | ENA

Control of Inflammatory Response by Tissue Microenvironment [RNA-seq]

Project description:Control of Inflammatory Response by Tissue Microenvironment [RNA-seq]

| PRJNA1120919 | ENA

Control of Inflammatory Response by Tissue Microenvironment [ChIP-seq]

Project description:Inflammation is an essential defense response but operates at the cost of normal functions. Whether and how the negative impact of inflammation is monitored remains largely unknown. Acidification of the tissue microenvironment is associated with inflammation. Here we investigated whether macrophages sense tissue acidification to adjust inflammatory responses. We found that acidic pH restructured the inflammatory response of macrophages in a gene-specific manner. We identified mammalian BRD4 as a novel intracellular pH sensor. Acidic pH disrupts the transcription condensates containing BRD4 and MED1, via histidine-enriched intrinsically disordered regions. Crucially, decrease in macrophage intracellular pH is necessary and sufficient to regulate transcriptional condensates in vitro and in vivo, acting as negative feedback to regulate the inflammatory response. Collectively, these findings uncovered a pH-dependent switch in transcriptional condensates that enables environmental sensing to directly control inflammation, with a broader implication for calibrating the magnitude and quality of inflammation by the inflammatory cost.

2025-06-03 | GSE269299 | GEO

Control of Inflammatory Response by Tissue Microenvironment [ChIP-Seq]

2025-03-20 | GSE269891 | GEO

Control of Inflammatory Response by Tissue Microenvironment

2025-03-20 | GSE269890 | GEO

Cellular microenvironment in inflammatory periapical tissue

Project description:Cellular microenvironment in inflammatory periapical tissue

| PRJNA811571 | ENA

Control of Inflammatory Response by Tissue Microenvironment [RNA-seq]

2025-06-03 | GSE269298 | GEO

Cellular microenvironment in inflammatory periapical tissue

Project description:Chronic apical periodontitis, typified by inflammatory granulation tissue formation and alveolar bone destruction, is the immune response around the apical root caused by long-term infection and pathogenic stimulation in the root canal. Through the recruitment and infiltration of immune cells and inflammatory mediators, wound healing begins accompanied by the starting of infection. Hence, a comprehensive understanding of biological processes and disease development from the cellular microenvironment in inflammatory periapical areas has important implications.

2022-03-31 | GSE197680 | GEO

The pulmonary inflammatory microenvironment at the time of exposure governs innate control of SARS-CoV-2 replication

Project description:SARS-CoV-2 (SCV2) infection leads to diverse clinical outcomes ranging from asymptomatic to fatal disease. Co-morbidities, age and host genetics together with immune status affect disease severity. However, the range of innate inflammatory pathways critical for limiting early viral replication and whether the inflammatory history and milieu of the lung microenvironment at the time of exposure impacts early control of SCV2 infection remain largely unexplored. Here, we investigated the roel of prior TLR stimualtion on early viral rpelciation in the lungs of K18 mice

2024-04-17 | GSE254993 | GEO

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